COLLEGE  OF   OSTEOPATHIC   PHYSICIANS 
AND  SURGEONS   •  LOS  ANGELES,  CALIFORNIA 


Oat. 


THE 

PHYSIOLOGY   OF   GOUT, 
RHEUMATISM,  AND  ARTHRITIS 


THE 

.PHYSIOLOGY  OF  GOUT, 

I — — - 

RHKUMATISM,  AND  ARTHRITIS 

AS    A    GUIDE    TO    ACCURATE     DIAGNOSIS 
AND     EFFICIENT    TREATMENT 


PERCY    WILDE,    M.D. 

l'/ivsician  to  the   Lans<i<wn  Hospital,  Bath 


XI-:  \V    YORK: 
WILLIAM     WOOD     AND     COMI'ANY 


MDCCCCXXII 


I'RINTF.I)    IN    KXGI.ANIJ    BY 
JOHN    WKIGHT    AND   SONS   LTD.,    BRISTOL 


PREFACE 

MY  medical  friends  have  frequently  asked  me  to 
explain  my  '  theories  '  of  Gout,  Rheumatism,  and 
Arthritis.  I  have  no  theories. 

Regarding  disorders  of  the  '  arthritic  '  class  not 
as  diseases  but  as  physiological  aberrations,  I  have 
endeavoured  to  ascertain  the  nafure  of  the  normal 
functions  and  the  results  which  happen  when  they 
are  imperfectly  performed. 

By  doing  so  I  find  myself  able  to  interpret  the 
symptoms  which  such  cases  present,  and  when  this 
has  been  done  the  appropriate  and  efficient  remedy 
for  the  individual  patient  suggests  itself. 

This  is  only  a  brief  summary  of  my  investiga- 
tions, but  I  hope  it  will  prove  helpful  to  the 
practitioner  and  enable  him  to  give  the  '  arthritic  ' 
patient  a  more  hopeful  outlook  than  has  hitherto 
been  possible. 

BATH,  PERCY    WILDE 

October,  1921 


26972 


CONTENTS 


CHAPTER  PAGE 
INTRODUCTION 

I.  SOME  CLINICAL  FACTS  9 

II.  THE  GENESIS  OF  THE  URATE  20 

III.  LACTIC  ACID  31 

IV.  THE  GENESIS  OF  THE  LITHATE  42 
V.  THH  GENESIS  OF  URIC  ACID  56 

VI.  EXCRETION  -  79 

VII.  RHEUMATISM  AND  THE  LACTIC-ACID  DIATHESIS  94 

VHI.  RHEUMATIC  FEVER  106 

IX.  PYRETIC  TREATMENT  117 

X.  GOUT   AND   THE    LlTHIC    DIATHESIS  132 

XI.  'ARTHRITIS'  150 

XII.  'NEURITIS'  193 

XIII.  THE  NURSE'S  PART  IN  TREATMENT      -  213 


The  Physiology  of  Gout, 
Rheumatism,   and  Arthritis. 


INTRODUCTION. 

THE  object  of  this  work  is  to  describe  the  methods, 
and  line  of  investigation,  which  have  enabled 
me  to  treat  successfully  a  large  number  of  disorders, 
commonly  described,  at  the  present  time,  as  '  arthritis  ' 
and  '  neuritis  ',  and  which  are  regarded  as  either 
intractable  or  incurable. 

It  may  be  expected  that  I  shall  begin  with  the 
announcement  that  I  have  discovered  some  drug 
which,  if  taken  continuously,  will  restore  the  joints 
and  the  tissues  to  their  normal  condition ;  or,  that  I 
have  invented  some  infallible  system  of  diet,  which  will 
prevent  the  poisons,  which  cause  such  destructive 
changes  in  the  joints,  from  being  manufactured  in  the 
body ;  or,  failing  this,  that  I  have  found  a  vaccine  fatal 
to  some  bacillus  which  I  have  proved  to  be  the  source 
of  all  the  mischief. 

I  have  done  none  of  these  things  ;  thirty  years'  ex- 
perience in  the  daily  treatment  of  such  cases,  and  much 
experimental  work,  has  not  encouraged  me  to  hope  for 
a  cure  from  any  of  these  methods.  It  is  true  that 
drugs  have  been  found  which,  because  they  relieve  some 
of  the  symptoms  met  with  in  such  cases,  have  raised 
hopes  that  a  true  specific  would,  at  length,  be  found; 

i 


2  INTRODUCTION 

but  centuries  have  passed  and  the  expectation  has  not 
been  realized. 

The  chemical  school,  as  a  result  of  numberless  ex- 
periments, concluded  that  an  excess  of  nitrogen 
introduced  into  the  body  was  a  serious  cause  of  joint 
trouble,  and  that,  by  severely  limiting  the  nitrogenous 
foods,  great  results  might  be  expected.  This  view  has 
been  very  generally  adopted,  with  the  result  that  for 
many  years  '  diet '  has  taken  the  place  of  the  '  weather ' 
as  a  subject  of  conversation  at  the  public  dinner-table, 
and  abstinence  from  certain  foods  has  been  raised  to 
the  level  of  a  virtue  by  some  people.  But  the  number 
of  those  who  suffer  from  '  arthritis '  has  not  diminished. 
During  the  war  we  took  thousands  of  men,  not  too 
well  fed,  and  of  no  great  physique,  and  we  crammed 
them  with  nitrogenous  foods ;  but  instead  of  developing 
joint  troubles  they  made  bone  and  muscle,  and  acquired 
powers  of  endurance  which  enabled  them  to  withstand 
the  severe  physical  strain  to  which  they  were  exposed. 

In  the  course  of  my  investigations,  I  had  to  examine 
the  two  processes  used  by  chemists  to  discover  the 
influence  of  foods  on  the  excretion  of  uric  acid.  I  found 
that  in  both  methods  a  very  remarkable  mistake  had 
teen  made,  which  I  shall  describe  in  the  chapter  on 
uric  acid.  I  found  that  in  the  solution  used  for 
estimating  the  quantity  of  uric  acid  there  was  none 
present,  and  the  only  nitrogenous  product  in  the  solu- 
tion was  added  by  the  chemist  in  the  course  of  his 
experiment  ! 

The  bacteriological  theory  which  is  now  widely 
accepted  makes  a  greater  appeal  to  the  imagination, 
because  we  know  that  certain  bacilli  are  responsible 
for  serious  mischief  to  joints.  Thus,  we  know  that 
the  gonococcus  bacillus  is  capable  of  producing  severe 


INTRODUCTION  3 

arthritic  symptoms,  and  that  these  may  continue  for  an 
indefinite  period.  To  a  lesser  extent  this  is  true  of  other 
bacilli,  such  as  the  staphylococcus  and  streptococcus. 

But  before  we  can  accept  the  view  that  these  bacilli 
are  the  primary  cause  of  the  joint  trouble,  we  have  to 
explain  how  it  happens  that  a  hundred  people  can  have 
their  tissues  invaded  by  the  gonococcus  bacillus  without 
developing  the  smallest  symptom  of  '  arthritis ' ;  and, 
when  we  come  to  other  bacilli,  they  may  be  found  in 
the  tissues  of  hundreds  of  people  before  we  come  upon 
a  case  where  arthritis  and  the  bacillus  are  co-existent. 

We  can  only  explain  this  by  saying  that  there  must 
exist  some  prior  condition  of  the  tissues  which  weakens 
their  resistance  to  the  attack  of  the  bacillus.  If  this  is 
true,  the  destruction  of  the  bacillus  will  only  relieve  the 
symptoms  it  causes,  and  not  the  condition  of  the  tissues 
upon  which  the  disorder  depends.  This  conclusion  is 
justified  theoretically,  and  also  by  the  results  of  efforts 
to  cure  the  disorder  by  the  use  of  vaccines. 

Thus,  in  chronic  rheumatism  we  find  that  in  the  large 
majority  of  cases  the  cause  is  prolonged  or  repeated 
exposure  to  cold. 

We  can  demonstrate  that  this  has  caused  an  impair- 
ment of  certain  normal  functions  of  the  body ;  that  this, 
in  turn,  has  caused  changes  in  the  normal  metabolic 
processes  of  the  body.  We  find  that  this  condition 
may  continue  for  a  long  period  before  any  symptom  is 
recognized  to  which  the  word  'rheumatic'  can  be 
applied.  But  during  this  time  there  is  a  gradual 
alteration  taking  place  in  the  fibrous  and  cartilaginous 
tissues,  and  it  is  only  when  these  have  made  considerable 
advances  that  the  early  symptoms  of  '  rheumatism '  are 
noted.  It  may  happen  that  during  the  whole  course 
of  the  disorder  no  symptom  of  fever  or  inflammation 


appears.  The  clinical  history  is  the  antithesis  of  the 
invasion  of  the  tissues  by  a  bacillus,  or  even  the 
administration  of  vaccines,  as  both  are  associated  with 
a  reaction  of  the  organism  and  an  elevation  of  the 
temperature  of  the  body. 

To  understand  how  some  simple  functional  impair- 
ment can  result  in  serious  changes  in  the  tissues,  it 
is  necessary  to  have  some  knowledge  of  the  normal 
metabolic  processes  and  the  conditions  which  govern 
their  mechanism.  In  studying  these  problems,  I  found 
very  little  help  from  either  physiological  text-books  or 
medical  literature. 

Sir  Michael  Foster,  in  his  great  work  on  physiology, 
concludes  his  chapter  on  metabolism  with  the  remark 
that  "  the  whole  story  of  proteid  metabolism  consists, 
at  present,  mostly  of  guesses  and  gaps  ".  As  far  as  I 
can  discover,  little  progress  has  been  made  since  this 
work  was  written. 

I  have  had  to  ascertain  the  facts  by  pefsonal  obser- 
vation and  experiment.  I  first  examined  the  human 
excretions  with  the  microscope,  under  varied  conditions  ; 
and  then,  in  order  to  find  out  the  chemical  composition 
of  the  crystals  observed,  I  used  the  method  of  synthesis 
instead  of  chemical  analysis.  That  is  to  say,  I  repro- 
duced these  crystals  artificially.  I  found  that  this 
not  only  gave  information  unattainable  by  chemical 
analyses,  but  also  prevented  me  from  falling  into  some 
mistakes  made  by  the  early  observers  and  which  have 
been  repeated  by  all  subsequent  writers.  In  fact,  the 
whole  uric-acid  theory  has  been  based  on  these  mistakes. 
My  difficulties  throughout  the  investigation  have  been 
less  with  the  normal  processes  of  nature  and  the  changes 
which  produce  these  disorders,  than  with  the  statements 
and  theories  which  have  been  so  long  and  so  universally 


INTRODUCTION  5 

accepted  as  basic  truths  that  it  appears  almost  impious 
to  reject  them. 

But  when  I  had  done  so,  the  obscurity,  which  has 
always  clouded  the  clinical  interpretation  of  the 
phenomena  presented,  disappeared,  and  it  became 
possible  to  find  a  physiological  explanation  of  every 
symptom  met  with  in  daily  practice.  I  found  that 
the  processes  of  metabolism  studied  by  the  method  I 
adopted  became  more  intelligible  and  less  intricate  than 
they  appeared  from  the  purely  chemical  standpoint,  and 
what  struck  me  most  was  the  evidence  of  purpose  and 
design  in  all  the  actions  and  reactions  observed.  I 
found  that  there  were  no  'waste  products',  that  each 
had  some  definite  duty  to  perform  necessary  to  the 
well-being  of  the  organism.  Thus  urea,  when  not  per- 
forming important  functions,  was  a  wholly  innocent 
body,  and  even  uric  acid  was  created  for  a  bene- 
ficent purpose. 

Metabolism  represents  unceasing  chemical  change  : 
but  what  surprised  me  was  how  little  these  changes 
were  influenced,  under  normal  conditions,  by  any  agent 
we  administer  either  as  drug  or  a  food.  The  most 
important  causes  of  chemical  change  are  purely  physi- 
cal, such  as  cold,  heat,  and  exercise  ;  and  because  it 
is  a  part  of  the  scheme  of  nature  that  this  should 
be  so,  these  changes  largely  take  place  in  the  great 
lymph-space  which  lies  immediately  beneath  the  skin 
throughout  the  whole  surface  of  the  body. 

We  all  know  how  much  the  symptoms  of  the 
rheumatic  patient  are  influenced  by  heat  and  cold,  rest 
and  motion  ;  but  we  do  not  always  realize  that  these 
symptoms  are  the  result  of  definite  chemical  changes 
taking  place  in  the  tissues. 

The  importance  of  this  large   lymph-space    is  very 


6  INTRODUCTION 

great,  and  a  knowledge  of  the  physiological  and  chemical 
processes  taking  place  in  it  are  necessary  before  we  can 
understand  the  nature  of  gout,  rheumatism,  or  arthritis  ; 
but  still  more  important  is  a  knowledge  of  the  special 
organs  designed  to  eliminate  the  metabolic  products  of 
our  tissues.  The  skin  has  been  described  as  regards  its 
structure,  its  capacity  to  regulate  the  temperature 
of  the  body  by  the  contraction  and  dilatation  of  its 
blood-vessels,  and  its  two  secretions,  one  of  sebaceous 
matter  and  the  other  of  sweat,  but  as  the  great  ex- 
cretory organ  of  the  products  of  tissue  metabolism 
it  is  practically  unrecognized. 

It  is  because  this  is  so,  that  physiologists,  looking  for 
the  results  of  muscular  metabolism  in  the  excretion  ot 
the  kidney  and  failing  to  find  it,  after  vigorous  exercise 
had  been  taken,  have  been  driven  to  invent  many 
speculative  theories. 

We  have  patients  becoming  hopeless  cripples  as  a 
result  of  an  impairment  of  its  functions.  We  may  have 
direct  clinical  evidence  that  a  chill  was  the  primary 
cause,  and  we  try  drugs,  diet,  and  vaccines  ;  and  because 
no  satisfactory  results  follow  our  efforts,  we  pronounce 
the  disorder  incurable. 

I  do  not  wish  to  convey  the  idea  that  the  skin  is  a 
mere  outlet  for  the  excretion,  and  that  its  channels 
may  become  clogged,  and  all  that  is  necessary  is  to  '  open 
the  pores  of  the  skin '.  The  functions  of  the  skin  include 
the  oxidation  of  the  waste  products  as  well  as  their 
excretion,  and  it  is  provided  with  all  the  machinery 
for  this  purpose.  We  may  obtain  excretion  from  the 
skin  without  restoring  its  functions. 

The  skin  does  not  merely  control  the  temperature  of 
the  body,  but  is  itself  a  source  of  heat.  For  this 
reason  functional  inactivity  of  the  skin  causes  the 


INTRODUCTION  7 

temperature  to  become  subnormal,  and  this  occurs  in 
men  otherwise  in  robust  health. 

But  while  a  restoration  of  the  function  of  the  skin 
is  a  primary  and  essential  condition  in  the  cure  of 
these  cases,  this  will  not  in  itself  cure  the  secondary 
changes  which  have  taken  place  in  the  tissues.  This 
involves  the  study  of  another  series  of  factors,  which 
we  are  helped  in  understanding  by  observing  the  pro- 
cesses which  nature  adopts  to  overcome  them. 

I  could  describe  a  very  large  number  of  cases 
diagnosed  as  '  rheumatoid  arthritis '  and  given  a  hopeless 
prognosis,  who  have  made  a  complete  recovery.  But 
if  I  gave  details  of  the  treatment  of  each  case,  I 
should  have  done  very  little  to  advance  our  knowledge 
of  the  subject.  The  term  'rheumatoid  arthritis',  as 
commonly  used,  conveys  no  information  as  to  the 
cause  of  the  disease,  the  constitutional  condition  of  the 
patient,  or  the  condition  of  the  affected  joints.  The 
treatment  indicated  in  one  case,  called  by  this  name, 
would  be  useless  or  of  little  advantage  in  another  case. 
\Yhen  I  read  theories  as  to  the  causes  of  'rheumatoid 
arthritis',  or  statements  respecting  remedies  found 
useful  in  its  treatment,  I  wonder  which  particular  class 
of  cases  the  writer  is  thinking  about ;  all  the  conditions 
differ  so  widely  in  cases  called  by  this  name  that  there 
is  no  scope  for  generalization. 

We  are  chiefly  concerned  in  such  cases  with  the 
restoration  of  the  functions  of  the  joints.  In  every 
case  of  joint  disease  there  is  only  one  line  of  treatment 
indicated  by  the  condition  of  the  joint,  and  unless  this 
is  followed  the  result  will  be  failure.  If  we  regard  any 
chronic  form  of  joint  trouble  merely  as  a  symptom  of 
a  disease,  and  try  to  treat  it  by  finding  a  remedy  for  the 
disease,  we  shall  be  almost  certain  to  neglect  the  obvious 


$  INTRODUCTION 

indications  for  treatment ;  thus,  the  patient  may  be 
allowed  to  walk  about  with  a  knee-joint  in  an  inflamed 
condition  while  we  are  treating  him  for  the  theoretical 
cause  of  the  disease.  We  cannot  say  that  any  particular 
treatment  is  indicated  for  different  varieties  of  joint 
trouble,  because  the  treatment  required  for  a  joint  at 
one  period  would  do  injury  to  the  same  joint  at  another. 

Neither  can  we  say  that  in  any  particular  case  the 
treatment  required  by  one  joint  or  more  would  be 
equally  valuable  for  all  the  joints  in  the  same  patient  ; 
on  the  contrary,  it  might  do  considerable  harm. 

The  proper  treatment  in  any  case  can  only  be 
ascertained  by  careful  physical  examination  of  the 
joint,  so  as  to  ascertain  the  exact  condition  of  its 
tissues  in  regard  to  the  processes  taking  place  in  them. 
Every  case  thus  becomes  a  physiological  problem,  and 
is  really  more  interesting  than  the  majority  of  cases 
with  which  the  physician  has  to  deal. 

It  is  to  help  the  practitioner  to  know  the  exact 
physiological  cause  of  the  symptoms  presented,  so  that 
he  may  be  able  to  apply  the  indicated  treatment,  that 
I  am  writing  this  book. 


CHAPTER    I. 

SOME     CLINICAL     FACTS. 

IT  is  a  natural  instinct,  when  we  see  a  patient  suffering 
the  pains  of  acute  gout  or  rheumatism,  to  seek  some 
remedy  which  will  quickly  relieve  his  sufferings.  To 
some  extent  we  have  it  in  our  power  to  do  so.  We 
may  give  colchicum  in  sufficiently  large  doses  to  relieve 
the  pain  of  acute  gout  and  shorten  the  attack.  But 
clinical  experience  teaches  us  that,  if  we  treat  gout  in 
this  way,  the  attacks  become  more  frequent  and  more 
severe,  and  there  is  a  concomitant  failure  in  health. 
The  abortive  treatment  of  acute  rheumatism  by  large 
doses  of  salicylates  is  followed  by  frequent  relapses 
and  prolonged  convalescence ;  and  heart  disease  occurs 
in  about  70  per  cent  of  the  cases  treated. 

These  results  happen,  not  because  there  is  anything 
peculiar  or  erratic  in  the  nature  of  these  diseases,  but 
because  we  have  used  language  which  conveys  a  false 
conception.  If  I  state  that  neither  rheumatism  nor 
gout,  regarded  as  diseases,  is  accompanied  by  pain, 
I  shall  not  be  understood,  because  we  have  become 
so  habituated  to  associating  the  symptoms  with  the 
disease.  But  we  shall  never  attain  success  in  the 
treatment  of  such  cases  until  we  recognize  the  difference 
between  the  symptom  and  the  disease.  The  word 
'disease'  can  only  be  properly  applied  to  any  agent 
or  condition  which  affects  the  functional  activity  or 
vitality  of  any  part  of  the  organism.  The  'symptom' 
is  produced  by  the  reaction  of  the  organism  against  this 


10  SOME    CLINICAL    FACTS 

agent,  or  the  failure  of  that  reaction  (secondary  sym- 
ptom). The  active  symptom  is  thus  a  force  moving 
in  an  opposite  direction  to  the  disease. 

The  pain,  swelling  of  joints,  and  fever  we  meet  with 
in  cases  of  gout  and  rheumatism  do  not  represent  the 
disease,  but  the  reaction  of  the  organism  against  it. 
The  disease  itself  has  none  of  these  symptoms,  but  one 
or  all  may  be  produced  by  the  effort  of  the  organism 
to  cure  the  disease.  Therapeutic  measures  have  failed 
in  these  disorders  because  the  misuse  of  language  has 
created  false  ideals. 

The  cause  of  the  disorder  may  exist  in  the  organism 
for  months  or  years  without  producing  symptoms,  but 
if  it  does  they  may  not  be  the  symptoms  usually 
associated  with  the  words  gout  and  rheumatism.  Thus 
many  cases  of  rheumatic  fever  escape  recognition 
because  the  joint  symptoms  usually  associated  with 
the  disease  are  absent. 

The  efforts  of  the  organism,  represented  by  the 
symptoms,  are  very  frequently  incomplete  because  the 
power  of  vital  resistance  is  limited  ;  but  if  we  mistake 
these  efforts  for  the  disease  and  endeavour  to  suppress 
them,  we  range  ourselves  on  the  side  of  the  disease  and 
allow  it  to  win  the  battle.  The  organism  may  make 
fresh  efforts,  after  a  time,  when  the  forces  we  have 
brought  to  bear  against  its  resistance  have  been 
removed,  and  then  we  call  it  'a  relapse';  or  we  may  so 
greatly  diminish  the  power  of  vital  reaction  that  the 
disease  becomes  symptomless,  whilst  it  is  working  that 
mischief  on  the  heart  or  kidneys  which  the  organism 
and  the  protective  powers  of  nature  were  trying  to 
avert. 

Thus,  in  the  eighteenth  century,  a  foreign  Convent 
prepared  a  powder,  of  which  one  dose  taken  every 


. 

SOME    CLINICAL    FACTS  11 

night  for  a  year  quite  arrested  the  attacks  of  gout  in 
those  suffering  from  the  disease.  The  Duke  of  Portland 
purchased  the  recipe  for  a  large  sum  of  money,  and 
presented  it  to  suffering  humanity.  But  it  was  found 
that  the  freedom  from  the  attacks  of  gout  usually 
resulted  in  death  from  disease  of  the  kidney.  Dr. 
Falconer,  of  Bath,  wrote  describing  his  experiences 
with  this  remedy  in  the  Medical  Journal  towards  the 
end  of  the  same  century,  and  as  a  result  its  use  was 
given  up  by  British  practitioners  and  has  long  since 
been  forgotten.  But  its  employment  has  been  revived, 
and  I  have  personally  seen  two  deaths  from  nephritis 
as  a  result  of  its  •  use.  The  rheumatic-fever  patient 
may  make  a  brilliant  recovery  from  the  acute  attack 
as  a  result  of  large  doses  of  the  salicylates,  subse- 
quently to  lead  an  invalid  life,  and  finally  die  of  heart 
disease. 

Not  only  is  it  important  to  recognize  symptoms 
and  diseases  as  forces  moving  in  opposite  directions, 
but  it  is  necessary  to  remember  that  a  similar  re- 
lation exists  in  the  medicinal  and  physical  agents  we 
employ  in  treatment.  This  is  obscured  in  our  works  on 
therapeutics,  because  writers  describe  the  symptoms 
produced  by  medicinal  agents  as  the  'action'  of  the 
drug. 

If  we  except  a  limited  number  of  drugs  which 
enter  into  chemical  combination  with  protoplasm,  and 
may  therefore  be  regarded  as  chemically  active,  we 
may  say  that  all  drugs  act  as  physical  stimuli,  and  the 
symptoms  they  produce  are  due  to  the  reaction  of  the 
organism  and  represent,  therefore,  a  force  moving  in 
an  opposite  direction  to  the  drug.  The  'action'  of  a 
drug  is  governed  by  physical  laws,  and  this  action  will 
increase  in  intensity  as  the  dose  is  augmented.  The 


12 

'  effects '  produced  by  drugs  are  governed  by  the  physio- 
logical laws  of  stimulation  and  exhaustion.  Any  agent 
which  can  stimulate  an  organic  element  has  also  the 
power  to  exhaust  it,  so  that  a  physical  agent  setting 
up  an  'action'  which  is  a  force  moving  in  one  direction 
with  increasing  intensity,  can  produce  effects  which  are 
exactly  the  reverse  of  one  another. 

It  is  a  fact  that  light  stimulates  the  sense  of  sight, 
and  sound  that  of  hearing ;  but  it  is  not  a  truth  unless 
we  also  state  that  excess  of  the  action  of  light  has  the 
effect  of  blinding,  and  that  excess  of  sound  is  deafening. 

It  is  important  that  we  should  keep  these  facts  before 
us.  Thus,  when  we  use  heat  to  stimulate  the  functions 
of  the  skin,  we  must  not  forget  that  excessive  heat  may 
seriously  impair  its  functional  capacity.  The  galvanic 
current  has  an  action  which  stimulates  the  activity  of 
the  nervous  system,  but  by  no  agent  can  we  so  quickly 
cause  its  exhaustion. 

Clinical  experience  helps  us  to  avoid  some  of  the 
evils  which  would  result  from  failure  to  recognize  these 
elementary  facts.  We  do  not  try  to  relieve  the  heat 
and  swelling  of  a  joint  afflicted  with  acute  gout  by 
plunging  it  into  cold  water  ;  we  have  learned  that 
such  treatment  would  be  disastrous.  On  the  contrary, 
we  wrap  up  the  affected  joint  and  increase  the  heat 
and  the  swelling  ;  and  in  doing  so  we  are  using  agents 
which  are  moving  in  the  same  direction  as  the  reaction 
of  the  organism,  and  therefore  we  know  that  a  right 
course  is  being  taken. 

But  the  conditions  we  meet  with  in  everyday  practice 
are  so  varied  that  we  cannot  depend  upon  our  own 
clinical  experience  or  that  of  others ;  for  guidance  we 
must  have  some  definite  principles  to  enable  us  to 
elucidate  the  problems  presented  and  enable  us  to  take 


SOME    CLINICAL    FACTS  13 

the  right  course.  Neither  the  recognized  routine  treat- 
ment, nor  the  results  of  the  clinical  experience  of  others, 
can  be  accepted  as  a  safe  guide.  The  gap  in  the  hedge 
may  appear  the  best  way  out  of  the  difficulty  ;  but  even 
if  this  gap  has  been  used  by  generations  of  others  until 
it  has  become  a  well-trodden  road,  unless  it  leads  us  to 
our  goal  we  must  fall  back  on  first  .principles  to  help 
us  to  seek  another  way. 

Thus,  the  symptoms  of  acute  gout  have  been  known 
and  recorded  since  the  beginning  of  history.  The 
patient  is  suddenly  seized  with  violent  pain  and  acute 
inflammation  in  one  or  more  joints  which  were  appar- 
ently healthy  at  the  moment  of  the  attack.  The  ancients 
took  the  view  that  this  was  due  to  some  morbid  matter 
in  the  blood  which  was  suddenly  instilled  into  the  joint. 
.  Rodulfe  in  the  thirteenth  century  crystallized  this 
theory  by  giving  this  disorder  the  name  '  gout ',  from  the 
French  '  goutte ',  a  drop,  to  signify  that  the  poison 
entered  the  joint  drop  by  drop.  This  view  has  been  so 
universally  adopted  that  we  can  express  the  attack  in 
practically  any  language  by  using  the  word  in  that 
language  which  is  equivalent  to  '  a  drop  ;. 

This  view  embodies  two  clinical  conceptions:  first, 
that  a  healthy  joint  is  liable  to  be  attacked  with 
acute  gout ;  secondly,  that  the  poison  which  causes 
the  inflammation  is  derived  from  the  blood.  The  whole 
literature  of  gout  has  been  built  upon  this  foundation. 
The  variations  which  occur  in  the  writings  of  successive 
centuries  have  been  as  to  the  exact  nature  of  the  poison 
which  exists  in  the  blood,  and  the  best  methods  of 
preventing  its  collection  or  of  eliminating  it  when 
collected.  What  evidence  have  we  that  these  clinical 
observations  are  true  ? 

The  first  conception  rests  entirely  upon  the  evidence 


14  SOME    CLINICAL    FACTS 

of  the  patient.  For  two  thousand  years  he  has  told 
the  physician  that  his  joint  was  quite  healthy  at  the 
moment  of  the  attack,  and  for  two  thousand  years 
the  physician  has  believed  him. 

Is  the  patient  a  credible  witness  ?  My  first  investi- 
gations into  the  nature  of  gout,  undertaken  about  thirty 
years  ago,  had  reference  to  this  point.  I  examined  the 
joints  of  a  very  large  number  of  persons,  regardless 
of  age  and  sex,  who  had  no  symptoms  of  gout  or  any 
trouble  with  the  joints.  I  was  surprised  at  the 
frequency  with  which  I  discovered  that  fine  crepitation 
which  indicates  the  presence  of  foreign  matter  in  or 
around  the  joints. 

The  usual  term  for  these  tiny  concretions  is  '  urates ' ; 
but  they  were  formerly  called  '  lithates ',  and  I  shall  use 
the  latter  word,  not  because  I  am  old-fashioned,  but 
because  it  does  not  commit  me  to  any  theory  of  the 
chemical  nature  of  these  concretions. 

The  patients  who  had  '  lithates  '  in  their  joints  were 
for  the  most  part  wholly  unconscious  of  the  fact. 
Therefore  the  statement  of  a  patient  that  his  joint 
was  perfectly  healthy  at  the  moment  of  the  attack  is 
valueless.  I  made  careful  note  of  the  position  and 
size  of  these  lithates,  and  I  had  the  opportunity  in 
many  cases  of  watching  their  history  over  a  long  term 
of  years.  In  some  cases  the  lithates  spontaneously 
disappeared.  I  have  seen  cases  where  a  few  days'  rest 
in  bed  would  produce  a  crop  of  lithates,  but  these 
would  disappear  directly  the  patient  resumed  active 
exercise.  In  many  cases  these  lithates  would  remain 
for  many  years  and  give  no  indication  of  their  pre- 
sence, but  in  some  cases  they  would  increase  in  size 
and  give  audible  evidence  of  their  existence  without 
causing  pain.  In  other  cases  a  certain  amount  of 


SOME    CLINICAL    FACTS  15 

irritation  was  set  up  during  movement  by  their 
mechanical  effects. 

I  became  accustomed  to  regard  all  persons  who  had 
this  tendency  to  deposit  lithates  in  their  joints  as  hav- 
ing the  '  lithic  diathesis  '.  I  took  particular  note  of  the 
physiological  conditions  and  symptoms  presented  by 
these  patients.  I  called  all  joints  where  lithates  were 
present  '  lithic  joints',  and  I  use  the  term  even  when 
pain  exists,  if  the  pain  is  due  to  purely  mechanical 
irritation. 

But  in  some  of  these  patients  the  lithates  underwent 
chemical  change  ;  there  was  pain  in  or  around  the  joint, 
the  severity  of  which  depended  upon  the  degree  of 
chemical  activity  which  was  taking  place.  When  it  was 
very  rapid  and  complete,  the  patient  exhibited  the  sym- 
ptoms of  acute  gout.  I  call  all  these  manifestations  of 
inflammatory  changes  produced  by  the  decomposition 
of  the  lithates  '  lithitis ',  and  use  the  adjectives  acute, 
subacute,  and  chronic  to  qualify  it. 

I  use  these  names  because  it  is  very  difficult  to 
describe  the  symptoms  we  constantly  meet  with  without 
a  better  nomenclature  than  we  possess,  one  which  often 
commits  us  to  false  theories  of  the  nature  of  the  dis- 
order. I  can  say  as  the  result  of  my  observations  that 
it  is  absolutely  impossible  for  any  healthy  joint  to  be 
attacked  with  gout.  The  lithates,  the  decomposition  of 
which  cause  the  attack,  have  existed  for  months  or  years 
before. 

I  have  read  statements  made  by  writers  on  gout  that 
the  deposits  are  due  to  the  attack  of  gout  and  increase 
with  the  recurrence  of  the  attacks.  This  statement  is 
based  upon  defective  observation.  In  every  case  the 
lithates  present  are  greatly  reduced  in  size  by  the  attack, 
but  in  no  case,  as  far  as  I  have  had  experience,  do  the 


16  SOME    CLINICAL    FACTS 

'tophi'  wholly  disappear  as  a  result  thereof.  This 
point  is  of  clinical  and  physiological  interest,  and  I 
will  explain  the  reason  for  it  later. 

At  this  stage,  I  can  reasonably  expect  that  others 
will  examine  the  joints  of  healthy  persons  to  see  whether 
lithates  can  be  found  as  frequently  as  I  have  described. 
It  is  necessary,  therefore,  to  describe  what  I  mean  by 
the  examination  of  a  joint.  We  may  inspect  a  joint, 
palpate  it,  or  have  an  x- ray  photograph  taken  of  it, 
and  we  may  obtain  much  valuable  information  as  a 
result,  but  we  have  not  placed  ourselves  in  a  position 
to  give  an  accurate  diagnosis  of  its  condition  until 
we  have  examined  it  during  the  performance  of  its 
functions.  I  could  describe  large  numbers  of  cases 
where  very  serious  errors  of  diagnosis  have  been  made 
because  this  fact  was  not  recognized. 

If  the  palm  of  the  left  hand  or  the  palmar  surface  of 
the  fingers,  according  to  the  size  of  the  joint,  is  pressed 
firmly  on  a  joint,  and  then  with  the  right  hand  the 
joint  is  put  through  the  extreme  movements  of  which 
it  is  capable,  the  smallest  deviation  from  the  normal 
condition  is  at  once  communicated  to  the  hand,  and  by  a 
little  manipulation  the  exact  site  can  be  located.  The 
fine  or  coarse  crepitation  of  lithates  is  unmistakable, 
and  conveys  an  accurate  idea  of  their  size,  while  the  soft 
creak  which  results  from  destruction  of  tissue  is  very 
evident.  The  sounds  can  be  accentuated  by  causing 
the  patient  to  make  the  movement  of  the  joint  while 
resistance  is  offered  to  it.  The  hand  soon  becomes 
educated  to  the  smallest  deviation  from  the  normal,  and 
it  becomes  unnecessary  to  remove  the  patient's  clothes 
when  examining  a  joint,  unless  other  conditions  render 
this  essential. 

We  now  come  to  the  second  proposition,  the  relation 


SOME    CLINICAL    FACTS  17 

of  the  chemical  constituents  of  the  blood  to  the  attack 
of  gout. 

If  we  agree  that  the  lithatcs  exist  in  the  joint  for 
months  or  years  before  the  attack,  is  the  blood  respon- 
sible for  their  deposition  ?  The  universal  opinion  of 
the  profession  is  in  the  affirmative.  Personally,  I 
think  no  single  practitioner  has  a  right  to  hold  that  view 
unless  he  is  in  a  position  to  explain  how  a  chemical  body 
so  highly  soluble  as  to  circulate  in  the  blood  can  sud- 
denly become  an  insoluble  body  when  it  reaches  certain 
tissues.  If  he  holds  this  view,  he  ought  to  be  able  to 
explain  further  how  the  insoluble  body  takes  such  a 
hold  on  the  tissues  that  all  the  great  forces  brought  to 
bear  upon  it  by  the  movements  of  the  joints  fail  to 
dislodge  it. 

This  subject  is  so  important  that  I  shall  devote  a 
special  chapter  to  its  consideration,  but  I  mention  it 
here  in  order  to  show  the  difficulties  in  which  we  are 
placed  if  we  adopt  theories  which  have  been  formulated 
on  the  'gap  and  guess  '  principle.  Clinical  evidence  is 
in  itself  often  misleading,  and  we  have  no  room  for 
theories  which  will  not  bear  investigation. 

Leaving  the  source  of  the  lithates  for  the  present,  we 
have  to  consider  whether  the  blood  is  directly  respon- 
sible for  the  chemical  change  taking  place  in  the  lithates 
which  produces  the  pain  of  gout.  Here  clinical  evidence 
may  lead  us  to  answer  the  question  in  the  affirmative. 
Every  practitioner  can  record  cases  where  the  pains  of 
gout  have  been  induced  by  eating  fruit,  or  drinking  port 
wine  or  beer,  or  by  too  much  '  red '  meat,  or  the  use  of 
sugar.  This  creates  the  impression  that  they  alter  the 
state  of  the  blood,  and  the  lithate  undergoes  decomposi- 
tion in  consequence.  But  large  numbers  of  lithic  patients 
can  take  any  or  all  of  these  things,  not  only  without 


18  SOME    CLINICAL    FACTS 

suffering,  but  to  their  great  advantage.  We  are  not  only 
confronted  with  this  problem,  but  with  one  that  is  much 
more  difficult  to  explain.  I  make  a  rule,  when  a  patient 
comes  to  me  with  lithitis  in  one  or  more  joints,  to 
examine  all  the  joints  of  the  limbs,  and  almost  in- 
variably I  find  that  the  lithates  are  not  peculiar  to 
the  joint  affected,  but  exist,  perhaps  in  greater  number, 
in  other  joints,  although  they  give  no  trouble  and 
the  patient  may  be  quite  unaware  of  their  existence. 
If  it  is  the  state  of  the  blood  which  has  set  up  the 
decomposition  of  the  lithates  in  one  joint,  why  does  the 
same  blood  have  no  effect  upon  the  lithates  in  the  other 
joints  ? 

This  is  not  a  momentary  matter ;  the  affected  joint 
may  continue  in  a  state  of  irritation  for  many  months, 
and  during  the  whole  of  that  period  the  lithates  in  the 
•other  joints  may  give  no  indication  of  their  presence. 
It  may  happen,  twelve  months  after  the  affected  joint 
has  become  quite  well,  that  these  other  lithates  com- 
mence to  undergo  decomposition,  and  the  symptomless 
joint  becomes  the  site  of  '  chronic  gout '. 

These  difficulties  have  led  to  the  idea  that  there  is 
-something  mysterious  and  difficult  to  understand  about 
gout ;  but  in  reality  it  is  the  theoretical  conclusions 
which  prevent  us  from  having  a  clear  conception  of  the 
nature  of  the  physiological  deficiencies  which  give  rise 
to  the  symptoms. 

In  the  treatment  of  all  disorders  of  the  gouty  and 
rheumatic  class  it  is  absolutely  necessary  that  we  should 
know,  not  only  the  physiological  causes  which  produce 
the  disorders,  but  also  the  exact  condition  of  the  patient 
at  the  moment  of  examination.  We  can  ascertain  these 
facts  by  knowing  what  happens  to  the  waste  products 
of  the  body  after  they  are  formed,  and  how  they  are 


SOME    CLINICAL    FACTS  19 

excreted.  It  will  be  found  that  in  the  study  of  meta- 
bolism this  subject  becomes  less  difficult  and  complex 
the  nearer  we  approach  the  truth.  We  can  by  certain 
tests  ascertain  the  exact  position  of  the  patient  in  regard 
to  these  processes  at  any  moment.  But  nothing  will 
take  the  place  of  accurate  physical  diagnosis,  because  we 
are  never  treating  an  abstract  name,  but  some  definite 
deficiency  or  series  of  deficiencies  in  the  individual 
patient,  and  these  will  not  be  the  same  at  any  two 
particular  periods  of  treatment.  Thus,  absolute  rest, 
and  vigorous  exercise,  may  be  essential  conditions  at 
different  stages  of  the  same  disorder,  and  when  to  order 
the  one  or  the  other  can  only  be  ascertained  by  careful 
physical  diagnosis.  The  symptoms  in  any  two  cases  are 
never  precisely  alike,  because  the  possible  combinations 
of  conditions  are  incalculable.  For  this  reason  there  can 
be  no  routine  treatment  suitable  for  even  a  large  propor- 
tion of  cases. 

There  is  really  no  class  of  cases  which  is  so  interesting 
to  study  or  so  much  worth  it,  because  in  the  past  they 
have  been  regarded  as  incurable. 

As  the  urate  is  credited  with  being  the  source  of  most 
of  the  troubles  of  gout,  I  will  give  it  the  first  consideration. 


20 


CHAPTER    II. 

THE    GENESIS    OF    THE    URATE. 

UREA  has  its  origin  in  the  dead  cell.  It  is  the  proto- 
plasm of  the  dead  cells  taken  as  food  which  constitutes 
the  largest  source  of  its  supply,  but  we  are  chiefly 
concerned  here  with  that  which  is  derived  from  the 
dead  cells  of  our  own  tissues. 

If  we  followed  the  ordinary  course,  and  considered 
the  d^ad  cell  after  it  had  been  resolved  into  its  chemical 
constituents  and  these  had  undergone  transformation, 
we  should  evade  one  of  the  greatest  physiological 
problems  with  which  nature  is  concerned,  and  fail  to 
understand  many  important  clinical  facts.  The  dead 
cell  is  an  insoluble  particle  of  organic  matter,  and  it 
occurs  in  aggregations  large  enough  to  block  the  capil- 
laries if  they  were  allowed  to  escape  into  the  circulation. 
The  dead  cell,  because  it  is  dead,  is  liable  to  undergo 
putrefaction. 

Here  are  two  difficulties  which  nature  has  to  meet 
in  the  normal  disposal  of  the  dead  cell,  in  every  tissue 
except  that  of  the  skin.  In  the  skin  it  does  not  matter ; 
the  dead  cell  has  only  to  dry  up  and  drop  off.  But 
even  this  description  as  regards  the  skin  is  not  cor- 
rect. If  we  bathe  the  skin  in  hot  water,  and  apply  soap, 
and  rub  it  dry  with  a  towel,  and  repeat  the  process  day 
by  day,  we  have  not  removed  the  dead  cells.  We 
can  prove  this  by  taking  a  vapour  bath  and  producing 
the  act  of  sweating.  If  we  now  rub  the  surface  of  the 
skin,  dead  cells  will  come  away  in  large  flakes,  which 


THE  GENESIS  OF  THE  URATE      21 

roll  up  as  we  pass  the  hand  over  the  skin.  This  shows 
that  the  dead  cell  is  not  only  firmly  adherent  to  the 
living  cell,  but  is  also  firmly  joined  at  its  edges. 

It  is  a  definite  physiological  law  that  the  dead  cell 
shall  remain  in  cohesion  to  the  living  cell  until  it 
has  undergone  such  chemical  change  as  will  render  it 
fit  for  removal.  The  delay  which  takes  place  in  the 
epithelial  cells  of  the  skin  does  not  appear  as  urgently 
necessary  as  it  must  be  for  the  cells  of  the  other  tissues. 
We  have  a  right  to  infer  that  what  we  know  actually 
takes  place  in  the  skin  must  take  place  in  the  dead  cells 
of  the  other  tissues.  We  may  go  further  and  say  that 
the  dead  cell  of  the  tissues  must  become  soluble  before 
it  is  removed  from  the  living  cell. 

If  this  conclusion  is  correct,  and  we  accept  the  teaching 
that  urea  is  formed  in  the  liver,  we  must  imagine  some 
other  soluble  nitrogenous  body  to  be  formed  before  it 
can  be  carried  to  the  liver.  As  urea  is  an  ultimate 
product  of  decomposition,  I  have  never  understood  the 
reason  for  supposing  that  some  special  organ  was 
responsible  for  its  manufacture.  The  dead  leaf  drops 
from  the  tree,  falls  to  the  ground,  and  becomes  resolved 
into  its  ultimate  constituents  without  the  aid  of  any 
special  organ  to  perform  the  work ;  why  should  it  be 
different  in  the  case  of  the  dead  cell  ?  It  has  been 
suggested  that  carbonate  of  ammonia  is  the  soluble 
nitrogenous  body  and  that  this  is  the  '  precursor  of 
urea' 

But  while  urea  is  constantly  being  converted  into 
ammonia  in  the  body,  there  is  no  evidence  to  show 
that  the  reverse  process  takes  place.  The  conversion 
of  ammonia  into  urea  is  not  an  easy  process  for  the 
chemist  to  accomplish.  Why  should  nature  adopt  the 
extremely  clumsy  method  of  making  carbonate  of 


22  THE    GENESIS    OF    THE    URATE 

ammonia  and  then  having  it  conveyed  to  the  liver  to 
be  converted  into  urea  ? 

In  order  to  study  the  physical  and  chemical  conditions 
of  the  dead  cell,  I  procured  some  of  the  tendons  of  an 
ox,  directly  after  it  was  killed.  I  selected  the  ox 
because  it  leads  a  sedentary  life,  and  the  metabolic 
changes  are  likely  to  be  slower.  It  was  necessary  to 
make  my  examination  immediately  after  death,  as  chem- 
ical changes  in  the  tissues  rapidly  follow.  I  used  the 
tendons  because  their  smooth,  white,  fibrous  tissue  has 
no  interstices  in  which  adventitious  matter  could  rest. 

I  placed  the  tendons  in  water  at  a  temperature  of 
100°  F.  for  half  an  hour.  I  then  decanted  the  fluid, 
and  found  it  was  slightly  opaque,  with  a  faint  yellow 
tinge.  Examination  under  the  microscope  revealed  a 
large  number  of  cells  showing  different  degrees  of 
disintegration.  These  were  dead  cells  which  had  been 
attached  to  the  living  tissue,  although  the  smooth 
glistening  appearance  of  the  tendon  gave  no  indica- 
tion of  their  presence. 

As  I  removed  these  cells  by  simply  immersing  the 
tendons  in  warm  water,  it  might  be  reasonably  asked 
why  they  were  not  removed  by  the  lymph  at  the  same 
temperature  during  life.  It  must  be  remembered  that 
a  change  takes  place  at  the  moment  of  death  which 
loosens  the  cohesion  of  the  dead  cell  to  the  living  tissue. 
I  shall  consider  the  nature  of  this  change  later.  This 
experiment  conclusively  proves  that  the  dead  cell 
remains  in  contact  with  the  living  tissue  until  its 
metabolism  is  complete. 

I  tested  the  solution  for  ammonia,  and  found  it 
absent,  because  the  animal  was  freshly  killed,  and  on 
testing  for  urea  with  hydrobromite  solution  I  found  it 
present  in  large  quantities. 


THE    GENESIS    OF    THE    URATE  23 

I  think  this  experiment  demonstrates  the  fact  that 
urea  is  formed  in  the  tissues  as  a  normal  product  of  meta- 
bolism, and  is  not  specially  manufactured  by  the  liver 
or  any  other  organ. 

I  found  in  my  solution  urea,  lactic  acid,  and  chlonde 
of  sodium,  in  addition  to  the  dead  cells.  Now  as  lactic 
acid  and  urea  have  a  great  affinity  for  one  another,  we 
might  suppose  that  they  existed  in  combination  as 
lactate  of  urea.  But  I  found  no  evidence  of  either 
lactate  of  urea  or  lactate  of  ammonia  in  my  solution. 
The  investigation  of  the  reason  for  this  gave  me  some 
unexpected  information  which  throws  a  great  light 
upon  the  problem  of  metabolism. 

Urea  has  the  formula  CO(NH.,)  „ ,  and  is  a  very  unstable 
body.  It  will  be  seen  that  it  only  requires  an  atom  of 
oxygen  to  convert  the  CO  into  carbonic  acid  gas,  and 
only  two  atoms  of  hydrogen  to  convert  the  (NH.,).,  into 
ammonia.  Thus  a  single  molecule  of  water,  if  its 
atoms  were  free,  would  convert  urea  into  carbonate  of 
ammonia. 

These  facts  convey  an  idea  of  the  chemical  nature  of 
urea,  but  we  are  concerned  here  with  the  great  affinity 
which  urea  has  for  acids.  It  forms  many  salts  which 
are  fairly  stable,  but  which,  when  decomposed,  yield 
ammonia  ;  but  in  the  human  body  the  acid  it  combines 
with  is  lactic  acid,  and  the  salt  formed  is  so  unstable 
that  we  never  find  it  in  the  excretions.  It  changes 
rapidly  into  lactate  of  ammonia.  Lactate  of  urea 
forms  crystals  which  resemble  long  slips  of  clear  glass. 
I  tried  to  photograph  some  which  I  made,  but  during 
the  process  they  became  decomposed,  and  the  photo- 
graph (Plate  I,  Fig.  i)  is  only  interesting  as  showing 
the  decomposition  taking  place. 

Urea  forms  long  silky  needles  as  we  find  it  outside 


24      THE  GENESIS  OF  THE  URATE 

the  body  (Plate  I,  Fig.  2),  but  under  no  circumstances 
do  we  find  a  crystal  of  urea  in  the  lymph  or  the 
excretions  of  the  body.  These  facts  bring  us  to  a  very 
important  source  of  confusion  in  the  whole  subject  of 
metabolism. 

The  endeavour  -has  been  made  to  express  physio- 
logical truths  in  the  language  of  chemistry,  and  the 
disadvantage  of  doing  so  is  shown  by  the  first  solution 
we  come  in  contact  with.  When  I  stated  that  I  found 
urea  in  my  solution,  I  used  chemical  language.  Urea  is 
there  because  it  answers  to  chemical  tests  ;  but  urea 
as  a  definite  crystalline  body  having  certain  affinities 
was  not  there,  otherwise  it  would  have  combined  with 
lactic  acid  and  formed  lactate  of  urea.  The  chemist 
takes  no  account  of  these  facts.  When  he  analyzes  a 
solution  of  Epsom  salts,  he  tells  us  that  it  contains  so 
much  sulphuric  acid  and  so  much  magnesium  ;  but  as 
a  matter  of  fact  the  sulphuric  acid  has  lost  its  hydrogen 
and  ceased  to  be  an  acid,  and  we  can  produce  none 
of  the  physiological  effects  of  sulphuric  acid  with  sul- 
phate of  magnesium. 

We  can  understand  urea  existing  in  the  blood  and 
the  lymph,  because  it  is  stable  in  an  alkaline  medium ; 
but,  How  can  it  pass  through  the  kidney  and  find  itself 
in  a  highly  acid  solution  and  not  become  converted 
into  ammonia  ?  I  do  not  think  that  anyone  has  ever 
asked  the  question  or  attempted  to  solve  it. 

The  chemist  proves  that  the  urine  contains  a  large 
amount  of  urea,  and  Sir  Michael  Foster  was  led  to 
believe  that  urea  had  an  independent  existence  in  the 
urine,  and  states  so.*  But  no  crystal  of  urea  is  ever 
found  in  the  urine,  and  it  would  be  impossible  for  it 

*  Text-book  of  Physiology,  p.   649. 


PLATE     7. 


Fig,  i- — Transformation  of  Lactate  of  Urea  into  Lactate  of  Ammonia. 


fig.  _'. — Urea. 


THE    GENESIS    OF    THE    URATE  25 

to  exist  in  the  urine  without  transformation  into  am- 
monia. In  the  same  way  urea  must  meet  free  lactic 
acid  in  the  lymph.  Why  does  it  not  combine  and 
become  converted  into  ammonia? 

This  points  to  the  fact  that  urea  must  enter  into 
some  chemical  combination  which  enables  it  to  resist 
the  action  of  acids,  and  a  clear  understanding  on  this 
point  is  absolutely  necessary  to  a  knowledge  of  the 
metabolic  processes.  Now  urea  exists  in  such  large 
quantities  that  we  pass  in  the  urine  about  512  grains 
every  day.  Therefore  any  body  which  combines  with 
urea  must  also  exist  in  large  quantities. 

This  directs  our  attention  to  chloride  of  sodium,  which 
occurs  in  such  abundance  in  the  fluids  of  the  body. 
Chloride  of  sodium  is  a  very  stable  salt,  but  viewed 
in  the  crystalline  form  has  a  remarkable  tendency 
to  change  its  appearance.  Various  forms  of  chloride  of 
sodium  are  illustrated  in  the  text-books.  From  the 
physiological  point  of  view  we  must  regard  every 
change  in  the  external  form  of  a  crystal  as  due  to 
some  alteration  in  its  chemical  composition,  and  there- 
fore we  must  look  upon  the  various  forms  in  which 
chloride  of  sodium  disguises  itself  with  some  suspicion. 
It  appeared  to  me  advisable  to  see  what  influence 
urea  had  on  the  formation  of  the  chloride  of  sodium 
crystals  contained  in  the  same  solution. 

I  made  a  solution  of  sodium  chloride  (4  gr.  to  the 
ounce)  in  distilled  water.  To  this  I  added  ^  gr.  of 
pure  urea.  This  was  placed  in  a  water-bath  at  100°  F. 
for  one  hour.  A  gas  was  evolved,  showing  that 
chemical  change  was  taking  place. 

A  drop  of  this  solution,  evaporated  and  examined 
under  the  microscope,  showed  that  the  normal  square 
crystals  of  chloride  of  sodium  had  disappeared,  and  that 


26 


THE    GENESIS    OF    THE    URATE 


crystals  of  the  'dagger'  type  had  taken  their  place. 
As  this  type  of  crystal  is  not  uncommon,  it  is  necessary 
to  observe  that  those  formed  by  the  combination  of 
urea  and  chloride  of  sodium  have  a  smooth  edge  and  a 
central  rib,  resembling  the  petal  of  a  flower  ;  and  many 
of  them  have  these  of  equal  length,  so  as  to  resemble  a 
flower  rather  than  a  dagger.  These  crystals  represent 
a  definite  chemical  body  composed  of  one  part  of  urea 
to  seven  parts  of  chloride  of  sodium.  It  is  not  a  double 
salt,  because  urea  is  not  a  salt ;  the  sodium  chloride  has 
not  been  decomposed,  but  as  a  gas  has  been  evolved 


Fig.  4. 


during  the  combination,  it  seems  probable  that  the 
urea  has  given  up  an  atom  of  hydrogen  in  the  process. 
This  point  I  have  not  determined  (Fig.  3). 

I  repeated  this  experiment,  using  urea  2  parts  to 
sodium  chloride  4  parts.  I  again  found  the  dagger- 
shaped  crystals  and  their  modification,  but  small  round 
crystals  appeared  dotted  about  between  the  larger 
crystals  (Fig.  4).  I  next  repeated  the  experiment,  using 
urea  2  parts  and  sodium  chloride  i  part.  The  result 
was  the  dagger  crystals  entirely  disappeared  and  the 
whole  field  was  covered  with  the  small  round  crystals 


PL  A  TE     II. 


THE    GENESIS    OF    THE    URATE  27 

which  had  only  appeared  in  a  limited  number  in  the 
former  experiment  (Plate  II,  Fig.  5).  These  experi- 
ments prove  beyond  question  that  urea  is  capable  of 
combining  with  chloride  of  sodium  in  all  proportions. 

I  had  made  a  number  of  crystals  which  corresponded 
exactly  with  those  I  met  with  in  the  body,  especially 
in  the  examination  of  sweat.  I  also  made  many 
intermediate  forms  which  result  from  the  combination 
of  urea  and  chloride  of  sodium  in  varying  proportion. 
I  have  not  described  these. 

I  next  dissolved  each  of  the  dried  microscopic  speci- 
mens in  a  |  per  cent  solution  of  lactic  acid.  When  they 
had  dried  again,  I  found  that  the  crystals  had  under- 
gone no  change  from  their  original  form.  I  found 
further  that  they  had  become  more  stable  and  less 
deliquescent  on  exposure  to  air.  I  then  understood 
how  urea  could  exist  in  the  presence  of  lactic  acid, 
without  being  converted  into  ammonia,  and  how  it 
could  resist  the  acids  it  met  with  in  the  urine. 

I  next  repeated  my  experiments  by  dissolving  urea 
and  chloride  of  sodium  in  distilled  water  rendered 
slightly  acid  by  the  presence  of  lactic  acid.  I  kept  the 
solution  in  a  water-bath  at  100°  F.  as  before,  but  I 
did  not  produce  a  chemical  combination  of  the  urea 
and  chloride  of  sodium  ;  instead  of  this,  the  urea 
combined  with  the  lactic  acid. 

In  this  way  I  discovered  a  very  important  fact. 
Urea  can  only  combine  with  chloride  of  sodium  in  an 
alkaline  or  neutral  solution.  If  sufficient  lactic  acid  is 
present  to  render  the  solution  even  slightly  acid,  the 
urea  combines  with  it  to  form  lactate  of  urea,  and 
becomes  rapidly  decomposed  into  lactate  of  ammonia. 

Now,  there  are  conditions  of  the  body,  especially 
during  active  exercise,  when  there  must  be  a  great 


28  THE    GEXESIS    OF    THE     URATE 

outpouring  of  lactic  acid  into  the  lymph,  but  yet  the 
lymph  preserves  its  alkalinity.  We  can  now  under- 
stand the  way  in  which  this  is  brought  about.  The 
lactic  acid,  by  its  combination  with  urea,  causes  the 
production  of  ammonia,  which  is  the  alkali  necessary 
to  preserve  the  balance. 

If  I  have  rightly  interpreted  my  experiments,  we 
should  expect  active  exercise  to  be  associated  with 
increased  excretion  of  ammonia.  I  shall,  in  another 
chapter,  show  that  this  result  actually  happens.  We 
are  thus  in  a  position  to  understand  better  the 
methods,  or  at  any  rate  one  of  them,  by  which  the 
alkalinity  of  the  blood  is  preserved.  We  can  also 
understand  another  point  :  ammonia  being  formed 
will  combine  with  any  fresh  lactic  acid  formed,  and 
this  combination  causes  the  evolution  of  heat.  We 
know  that  exercise  raises  the  temperature  of  the  body, 
and  this  must  be,  at  least,  one  of  the  sources. 

In  the  combinations  made  by  urea  with  chloride  of. 
sodium,  we  have  the  true  urate  of  the  body,  in  contra- 
distinction to  the  so  called  'urate  of  soda',  which  is  an 
alleged  combination  of  uric  acid  and  soda. 

There  is  no  evidence  of  the  existence  of  the  latter  salt 
in  the  body.  I  shall  show  that  the  crystals  described 
as  urate  of  soda  by  the  earlier  writers  contained  neither 
uric  acid  nor  soda.  The  true  urate  is  found  in  great 
abundance  in  the  lymph,  the  sweat,  and  the  urine  ; 
but  in  the  latter  it  exists  in  such  minute  crystals  that 
it  appears  difficult  to  prove  that  they  are  identical  with 
the  crystals  I  have  produced  by  the  combination  of 
urea  and  chloride  of  sodium.  The  crystals  in  the  urine 
are  very  minute,  because  urea  exists  there  in  great 
preponderance  over  chloride  of  sodium.  In  the  normal 
sweat  we  find  the  dagger-shaped  crystals  with  very 


THE    GENESIS    OF-    THE    URATE  29 

great  frequency,  because  the  chloride  of  sodium  exists 
in  great  excess  to  the  urea. 

This  fact  suggested  to  me  a  test  by  which  I  could 
assure  myself  that  the  minute  crystals  which  cover  the 
whole  field  when  a  drop  of  urine  is  evaporated  are 
identical  with  the  artificial  urates  I  had  made  by  adding 
an  excess  of  urea  to  chloride  of  sodium.  If  I  altered 
the  proportion  in  the  urine  so  that  chloride  of  sodium 
was  in  excess,  I  then  ought  to  be  able  to  produce  the 
dagger-shaped  crystals.  I  thereupon  added  chloride  of 
sodium  in  excess  to  a  specimen  of  urine  and  maintained 
it  at  100°  F.  for  thirty  minutes.  A  gas  was  given  off, 
showing  that  chemical  combination  was  taking  place.. 
On  evaporation  I  found  abundance  of  the  dagger 
crystals  in  the  field.  I  also  found  that  the  minute 
urates  had  disappeared.  They  had  become  disassoci- 
ated to  provide  the  urea  to  combine  with  the  larger 
amount  of  chloride  of  sodium.  (Plate  II,  Fig.  6.} 

This  is  a  very  complete  demonstration  of  the 
chemical  nature  of  the  urate.  The  knowledge  of  its 
composition  explains  some  of  the  gaps  left  in  the  story 
of  nitrogenous  metabolism.  It  explains  how  urea  can 
exist  in  the  lymph,  side  by  side  with  lactic  acid, 
without  being  converted  into  lactate  of  urea  and 
passing  into  ammonia.  The  urea  is  protected  by  its 
combination,  and  is  thus  able  to  pass  through  the 
kidneys  and  exist  in  the  urine  without  undergoing 
decomposition. 

The  fact  that  this  combination  cannot  take  place 
in  the  presence  of  free  lactic  acid,  when  the  free  urea 
combines  with  the  lactic  acid  and  becomes  converted 
into  ammonia,  explains  one  of  the  chief  methods  used 
by  nature  to  preserve  the  alkalinity  of  the  blood,  and 
also  explains  why  the  quantity  of  urea  is  diminished 


30      THE  GENESIS  OF  THE  URATE 

under  circumstances  in  which,  without  this  knowledge, 
we  should  expect  an  increase.  I  shall  refer  to  this 
question  later. 

We  shall  now  look  upon  urea,  not  merely  as  the 
final  result  of  nitrogenous  metabolism  and  the  possible 
cause  of  pathological  conditions,  as  a  product  which  we 
should  be  better  without,  but  as  an  agent  performing 
necessary  functions  and  acting  as  a  continual  safeguard 
against  the  grave  results  which  would  follow  if  the 
lymph  became  an  acid  solution. 


31 


CHAPTER   III. 

LACTIC     ACID. 

LACTIC  ACID  has  an  intensely  acid  reaction,  but  it 
exists  in  the  blood  and  the  tissues  without  disturbing 
their  alkalinity.  The  quantity  present  in  any  two 
individuals  differs  very  widely,  and  there  is  also  a 
great  variation  in  the  total  amount  present  in  any 
single  individual  at  different  times. 

Although  lactic  acid  circulates  with  the  blood,  the 
quantity  which  may  be  present  in  one  part  of  a  tissue 
at  any  moment  may  be  out  of  all  proportion  to  the 
quantity  contained  in  another  part  contiguous  to  it. 
This  acid  therefore  presents  us  with  many  points  of 
physiological  and  clinical  interest. 

The  physiological  text-books  do  not  give  us  much 
information  respecting  lactic  acid.  Sir  Michael  Foster 
(Text-Book  of  Physiology,  p.  826}  tells  us  : — 

"  The  products  of  muscular  metabolism  pass  into  the 
lymph  bathing  the  fibre,  and  so,  either  by  a  direct  path 
into  the  capillaries  or  by  a  more  circuitous  course  through 
the  general  lymphatic  system,  into  the  blood. 

"  The  fate  of  the  carbonic  acid  we  have  fully  treated  of 
in  dealing  with  respiration  ;  the  little  we  know  concerning 
its  nitrogenous  product  or  products  has  been  stated  in 
dealing  with  urea  ;  the  third  recognized  product  is  lactic 
acid  or  sarcolactic  acid.  Did  any  considerable  amount 
of  oxidation  take  place  in  the  blood-stream  while  the 
blood  is  flowing  along  the  larger  channels,  subject  only 
to  the  influence  of  the  vascular  walls,  we  might  fairly 
expect  that  the  lactic  acid  discharged  from  the  muscles 
would  be  subjected  to  oxidizing  influences  while  still  with- 
in the  blood-stream  of  the  larger  channels.  We  have, 


32  LACTIC    ACID 

however,  no  satisfactory  evidence  of  any  lactic  acid  being 
oxidized  in  this  way.  On  the  contrary,  there  is  a  certain 
amount  of  experimental  and  other  evidence  that  lactic 
acid  present  in  the  blood  is  somehow  or  other  disposed  of 
by  the  liver,  and  that  if  the  liver  fails  to  do  its  duty,  lactic 
acid  may  appear  in  the  urine." 

If  we  turn  to  modern  literature  and  consult  the 
writings  of  those  physicians  who  discuss  the  cause  of  an 
'  acid  condition  of  the  blood  '  and  its  effects  upon  the 
tissues,  we  find  that  they  are  so  interested  in  uric  acid, 
by  which  they  explain  all  the  symptoms,  that  'the 
existence  of  lactic  acid  is  ignored  altogether. 

This  adds  to  our  difficulties,  because,  while  we  cannot 
examine  an  animal  tissue  or  fluid  without  coming  in 
contact  with  lactic  acid,  if  we  want  to  investigate  the 
subject  of  uric  acid  we  must  turn,  not  to  the  human 
body,  but  to  the  literature  of  gout  and  uric  acid,  for 
information.  If  we  have  any  doubts  about  the  fact 
that  uric  acid  exists  in  the  blood  we  are  referred  to  an 
experiment  made  before  the  middle  of  the  last  century, 
which  is  regarded  as  convincing.  If  we  are  convinced, 
we  are  still  not  out  of  our  difficulties,  because  we  do 
not  know  what  happens  when  these  two  acids  meet 
one  another  in  the  tissues  or  in  the  blood.  There 
can  hardly  be  a  '  tug-of-war ',  because  lactates  have 
the  property  of  dissolving  uric  acid  and  therefore  must 
get  the  best  of  it.  The  older  physicians  attached  great 
importance  to  lactic  acid  as  a  cause  of  rheumatism 
and  kindred  diseases.  With  the  advent  of  the  uric- 
acid  theory,  lactic  acid  as  a  source  of  acidity  of  the 
blood,  and  as  an  irritant  to  the  tissues,  disappeared 
from  literature.  This  fact  is-  of  more  than  historical 
importance. 

We  can  obtain  much  valuable  knowledge  respecting 
lactic  acid  from  a  well-known  physiological  experiment. 


LACTIC    ACID  33 

The  legs  of  a  dead  frog  are  stimulated  by  an  inter- 
rupted faradic  current,  and  the  muscles  vigorously 
contract.  After  a  time  the  contraction  ceases.  It  is 
then  found  that  the  muscle  has  become  loaded  with 
lactic  acid.  If  we  wash  this  away,  and  again  apply 
the  current,  the  contraction  of  the  muscle  is  resumed. 
This  proves  to  us  that  lactic  acid  is  a  product  of 
muscular  metabolism,  and  that  it  accumulates  in  the 
muscle  during  fatigue  and  arrests  the  function  of  the 
muscle. 

We  are  not  on  such  sure  ground  when  we  come  to 
the  explanation,  viz.,  that  perfect  contraction  of 
muscle  evolves  carbonic  acid  gas,  and  that  when  the 
contraction  is  imperfect  lactic  acid  is  produced. 

We  may  have  a  series  of  the  most  vigorous  contrac- 
tion of  muscle  both  in  the  frog  and  the  human  being, 
and  still  lactic  acid  is  formed.  If  we  admit  that  lactic 
acid  is  a  product  of  imperfect  combustion,  we  cannot 
leave  out  of  account  the  fact  that  it  is  formed  when 
the  nerve  supplying  the  muscle  is  exhausted.  This 
point  is  of  clinical  importance. 

We  know  that  under  all  conditions  the  supply  of 
lactic  acid  is  maintained,  and  the  amount  is  increased 
by  exercise.  We  know  also  that  any  condition  which 
limits  the  circulation  in  a  tissue  may  lead  to  the 
accumulation  of  lactic  acid  in  that  tissue.  This  may 
be  the  result  of  cold  or  injury  either  to  the  tissues 
or  the  nerve  supplying  them.  Thus,  rheumatism  is 
likely  to  occur  in  a  joint  which  has  been  sprained 
many  months  before.  The  impairment  of  the  circu- 
lation remains  for  a  long  time  after  such  injuries. 

That  impairment  of  the  circulation  and  a  locally 
lowered  temperature  of  the  part  precede  the  rheumatic 
attack  in  such  cases  is  a  point  easily  demonstrable. 

3 


34  LACTIC    ACID 

We  may  say  that  the  power  of  lactic  acid  to  accumulate 
in  any  tissue  is  in  inverse  ratio  to  the  activity  of  its 
circulation.  This  is  a  clinical  fact  to  be  remembered. 

The  great  affinity  which  lactic  acid  has  for  the 
animal  tissues  may  be  demonstrated  by  placing  a  piece 
of  meat  or  tendon,  or — better  still  for  purposes  of 
demonstration — a  small  fish,  into  a  5  per  cent  solution 
of  lactic  acid.  After  it  has  been  there  for  a  few  hours, 
pour  off  the  lactic  acid,  and  wash  the  meat  or  fish  with 
cold  water  to  remove  the  lactic  acid  from  the  surface. 
We  can  prove  that  the  lactic  acid  has  invaded  every 
cell  in  the  tissues,  by  the  fact  that  the  fish  is  permanently 
preserved  against  putrefaction.  Thus  we  may  keep  it 
for  months  without  any  decomposition  taking  place, 
and  this  refers  not  only  to  every  tissue  of  the  fish  but  to 
the  contents  of  the  intestine.  This  also  demonstrates 
the  lact  that  one  of  the  functions  of  lactic  acid  is  to 
prevent  putrefactive  changes  taking  place  in  any  dead 
organic  matter  which  may  be  present  in  the  tissues. 

We  have  dead  organic  matter  in  the  form  of  the  dead 
cells,  and  that  lactic  acid  plays  a  part  in  their  removal 
we  have  seen  in  the  previous  chapter.  From  its  great 
affinity  to  the  tissues,  and  from  some  experiments  I 
shall  describe,  we  cannot  imagine  lactic  acid  existing 
in  the  lymph  without  invading  the  dead  cell,  and  be- 
cause it  does  so  it  preserves  it  from  putrefaction. 

Lactic  acid  is  usually  described  as  forming  salts  with 
zinc  and  calcium.  It  appears  to  have  escaped  attention 
that  a  large  proportion  of  the  salts  we  find  in  the  excre- 
tions are  either  lactates  or  contain  lactic  acid.  I  have 
already  mentioned  that  when  present  in  excess  it  can 
combine  with  urea  to  form  lactate  of  urea,  and  that  this 
becomes  transformed  into  lactate  of  ammonia. 

It    also   combines   with    chloride   of    ammonium    to 


LACTIC    ACID 


35 


form  lactochloride  of  ammonium.  I  have  never  seen 
chloride  of  ammonium  in  the  excretions ;  it  always 
appears  as  the  lactochloride. 

Lactic  acid  with  chloride  of  sodium  forms  rods  which 
appear  either  as  crosses  with  rods  of  unequal  length, 
or  as  a  long  rod  with  lateral  rods  at  right  angles  and 
of  unequal  length.  It  closely  resembles  the  lacto- 
chloride of  ammonium  crystal ;  both  these  are  very 
common  in  the  excretions  of  the  skin  (Fig.  7).  Lactic 
acid  forms  with  phosphate  of  lime  a  characteristic 
crystal  which  I  shall  describe  later.  Phosphate  of  lime 


never  occurs  in  the  body  except  as  a  lactophosphate. 

But  the  combinations  of  lactic  acid  have  certain 
peculiarities  which  it  is  necessary  to  understand  before 
we  can  interpret  certain  clinical  and  physiological 
results.  The  chemical  combination  alters  the  shape  of 
the  crystal,  and  after  that  has  taken  place  more  lactic 
acid  may  be  absorbed  into  the  crystal  without  any 
alteration  taking  place  in  its  form.  Thus  lacto- 
chloride of  ammonium  may  be  an  alkaline  salt  or  an 
acid  salt,  according  to  the  amount  of  lactic  acid  it 


36  LACTIC    ACID 

contains.  The  same  is  true  of  the  lactophosphate  of 
lime.  Some  part  of  this  lactic  acid  exists  in  chemical 
combination,  the  remainder  is  additive ;  it  remains 
in  the  crystal  in  a  state  of  physical  cohesion.  We 
can  illustrate  this  physical  condition  by  prolonged 
trituration  of  one  part  of  aniline  violet  with  1000  parts 
of  powdered  glass.  We  shall  then  have  a  pale  lavender- 
coloured  powder,  which  may  be  placed  in  water  and 
kept  there  indefinitely  without  any  solution  of  the  aniline. 
This  is  because  the  energy  of  the  cohesion  between  the 
particles  of  the  aniline  and  the  glass  is  greater  than 
the  energy  of  the  water  to  overcome  this  cohesion. 
Now  if  we  supply  energy  in  the  form  of  heat,  and  boil 
the  water  in  which  the  aniline  trituration  is  placed, 
the  energy  of  cohesion  is  overcome  and  the  aniline  is 
dissolved  and  colours  the  solution.  I  think  this  exactly 
represents  the  physical  condition  of  the  surplus  lactic 
acid  in  the  salt.  If  we  supply  energy  in  the  form  of 
heat,  we  release  the  lactic  acid  from  its  cohesion  and 
set  it  free. 

If  we  take  the  fish  which  we  have  caused  to  contain 
an  excess  of  lactic  acid  in  a  state  of  physical  cohesion, 
and  we  place  it  in  a  solution  of  phenolphthalein  which 
has  been  made  red  by  the  addition  of  soda,  we  shall 
find  that  this  fish,  charged  with  an  intensely  acid  body, 
does  not  alter  the  alkalinity  of  the  solution.  It  still 
remains  red.  Now  if  we  apply  heat  to  the  solution, 
the  lactic  acid  will  be  set  free  and  the  colour  will  be 
discharged  from  the  solution  in  consequence. 

This  experiment  also  explains  how  it  happens  that 
an  intensely  acid  body  like  lactic  acid  can  exist  in  the 
lymph  without  altering  its  alkalinity. 

Lactic  acid  is  a  very  hygroscopic  fluid,  but  its  action 
on  animal  tissue  is  to  make  it  lose  its  natural  moisture 


LACTIC    ACID  37 

and  to  become  rigid.  It  does  this  without  effecting 
any  alteration  in  the  structures  of  the  tissues  it  invades. 
This  stiffness  of  the  muscle  is  met  with  in  practice  under 
two  conditions  :  one  is  after  severe  exercise,  the  other 
a  short  time  after  death.  We  call  the  latter  condition 
'  rigor  mortis  '.  Both  are  due  to  the  action  of  lactic 
acid  on  the  tissues. 

'  Rigor  mortis '  is  ascribed  to  coagulation  of  the 
myosin  of  the  muscle,  but  this  explanation  does  not 
account  for  its  subsequent  sudden  disappearance.  We 
know  that  death  releases  a  large  amount  of  lactic  acid 
which  has  been  locked  up  in  the  tissues,  and  this  free 
acid  will  at  once  invade  the  muscular  and  fibrous  tissues 
as  it  did  in  my  experiments.  It  thus  produces  the 
rigidity  which  is  one  of  its  characteristic  effects.  But 
it  will  also  subsequently  combine  with  the  urea  to  form 
lactate  of  urea,  and,  as  this  decomposes,  ammonia  is 
formed,  the  lactic  acid  is  again  locked  up  as  lactate  of 
ammonia,  and  the  rigidity  disappears. 

In  the  stiffness  of  the  muscles  which  occurs  after 
severe  exertion,  the  lactic  acid  becomes  gradually 
oxidized,  and  as  it  does  so  the  stiffness  disappears  ; 
but  owing  to  the  increased  acidity  produced  by  the 
process  of  oxidation,  the  tissues  become  tender,  and 
there  is  pain  on  movement.  It  may  take  twenty-four 
hours  before  these  symptoms  appear,  and  sometimes 
longer  ;  it  may  be  some  days  before  the  process  is 
completed  and  normal  conditions  are  resumed. 

As  the  excretions  contain  so  many  lactates,  it  follows 
that  lactic  acid  must  be  a  normal  constituent  of  the 
urine.  But  lactic  acid  is  never  included  in  the  chemical 
analysis  of  urine.  It  is  described  as  sometimes  existing 
in  the  urine  under  abnormal  conditions.  It  is  extra- 
ordinary that  although  the  urine  has  formed  the  subject 


38  LACTIC    ACID 

of  continuous  chemical  experiment  for  a  century,  and 
most  of  our  knowledge  of  nitrogenous  metabolism  is 
derived  from  these  experiments,  the  ingredient  which 
is  of  distinctly  the  greatest  clinical  importance  has 
escaped  observation  altogether  ;  on  the  other  hand, 
uric  acid  is  regarded  as  a  normal  constituent,  although 
it  is  a  physical  impossibility  for  uric  acid  to  exist  in 
the  urine,  except  in  minute  quantities,  because  of  its 
insolubility.  It  is  obvious,  without  any  chemical  test 
being  made,  that  the  urine  must,  normally,  contain 
lactic  acid. 

Uffelmann's  test,  which  is  a  i  per  cent  solution  of 
carbolic  acid,  with  sufficient  ferric  chloride  to  produce 
a  purple  colour,  is  the  recognized  test  for  lactic  acid. 
If  a  drop  of  this  solution  be  added  to  a  drop  of  urine 
the  colour  immediately  disappears.  But  this  test  is 
not  altogether  convincing  when  used  in  such  a  com- 
plex chemical  compound  as  the  urine.  I  have  devised 
another  test  which  is  both  interesting  and  instructive. 
Knowing  the  peculiar  affinity  which  lactic  acid  has  for 
animal  tissue,  I  placed  a  piece  of  meat  in  some  urine 
and  allowed  it  to  remain  for  some  hours.  I  then 
removed  the  meat  by  the  piece  of  string  I  had  placed 
round  it,  and,  after  washing  it  under  the  tap,  hung  it 
up  to  dry.  Although  it  was  hot  weather,  and  the 
meat  was  fully  exposed,  it  showed  no  symptoms  of 
putrefaction.  It  became  dry  and  rigid  as  all  animal 
tissues  do  which  are  immersed  in  a  lactic  acid  solution. 
This  is  a  conclusive  proof  that  lactic  acid  exists  in  the 
urine  and  in  large  quantities.  Incidentally  this  experi- 
ment shows  that  the  affinity  of  lactic  acid  for  animal 
tissue  is  stronger  than  its  affinity  for  the  salts  with 
which  it  is  in  additive  combination.  The  large  amount 
abstracted  shows  that  it  could  not  have  existed  in 


LACTIC    ACID  39 

chemical  combination.  Some  months  later  I  used 
this  piece  of  meat  for  another  interesting  experiment. 
I  added  sufficient  soda  to  a  solution  of  phenolphthalein 
to  give  it  a  brilliant  red  colour.  I  placed  my  meat 
in  the  solution  and  left  it  there  for  six  hours.  There 
was  no  change  in  the  colour  of  the  solution,  showing 
that  the  lactic  acid  was  locked  up  by  its  combina- 
tion with  the  meat.  This  was  a  repetition  of  the 
experiment  I  have  already  described  when  meat  was 
soaked  in  a  5  per  cent  solution  of  lactic  acid,  but 
it  gives  further  proof  that  lactic  acid  had  been  ab- 
stracted from  the  urine.  I  then  tested  the  further 
characteristic  of  lactic  acid  by  heating  the  solution. 
When  I  had  applied  considerable  heat,  the  colour  of 
the  solution  disappeared,  showing  that  lactic  acid  had 
been  given  off.  I  left  the  meat  in  the  solution,  and 
was  surprised  to  see  the  next  morning  that  the  red 
colour  had  returned  to  it,  the  solution  having  resumed 
its  alkalinity.  The  lactic  acid  had  evidently  gone  back 
to  the  meat  as  the  solution  cooled.  A  very  small 
amount  of  heat  was  necessary  this  time  to  set  free  the 
lactic  acid  again. 

This  is  a  very  remarkable'  demonstration  of  the 
physical  affinity  which  two  substances  may  have  for 
one  another,  and  the  way  in  which  chemical  changes 
can  be  produced  by  purely  physical  causes. 

These  experiments,  in  addition  to  proving  that 
lactic  acid  exists  in  large  quantities  in  normal  urine, 
show  how  easily  we  can  manipulate  lactic  acid  and  free 
it  from  its  additive  combinations,  by  heat. 

There  is  another  simple  test  for  the  presence  of  lactic 
acid  in  urine  based  on  the  same  principle  as  the  last. 
A  solution  of  phenolphthalein  is  added  to  the  urine,  and 
then  sufficient  soda  to  render  the  urine  alkaline,  so 


40  LACTIC    ACID 

that  a  red  colour  is  produced.  If  the  urine  is  now 
heated,  lactic  acid  is  set  free  and  its  red  colour  dis- 
appears. I  do  not  think  that  the  fact  that  the  acid 
reaction  of  the  urine  is  increased  by  heat  has  been 
hitherto  observed. 

I  have  described  the  physical  effect  which  lactic  acid 
has  upon  animal  tissues,  how  it  causes  them  to  become 
stiff  and  rigid,  and  this  condition  is  permanent.  On 
the  other  hand,  we  have  seen  that  when  lactic  acid 
invades  the  living  muscles,  the  stiffness  it  produces 
disappears  in  a  little  while,  and  is  followed  by  more'  or 
less  tenderness  and  pain  in  the  part.  Also  that  when 
lactic  acid  is  set  free  in  the  body,  after  death,  it  causes 
a  rigidity  of  the  muscles  which  we  call  the  '  rigor 
mortis',  and  this  disappears  as  soon  as  the  lactic  acid 
has  been  locked  up  again  by  its  combination  with 
ammonia. 

It  might  be  thought  that  we  might  expect  the  same 
thing  to  occur  in  the  dead  tissue  we  have  immersed 
in  lactic  acid,  especially  as  lactate  of  ammonia  is  formed 
in  that  tissue.  But  we  must  remember  that  the  quantity 
of  urea  existing  in  the  tissue  is  limited,  and,  when  all 
of  it  has  been  used  to  make  lactate  of  ammonia,  the 
quantity  of  lactic  acid  is  not  sufficiently  diminished 
to  materially  alter  its  physical  effect  upon  the  tissues. 

Now  if  we  are  influenced  by  the  fundamental 
physiological  error  which  leads  us  to  suppose  that 
every  agent  is  only  capable  of  producing  one  effect 
or  series  of  effects  upon  the  organism,  and  these  effects 
can  be  increased  by  augmentation  of  the  dose,  we 
should  expect  that  we  could  increase  the  rigidity  of  the 
tissue  by  using  a  stronger  solution  of  lactic  acid.  If, 
instead  of  a  5  per  cent  solution,  we  used  one  of  25  per 
cent,  and  immersed  a  small  fish  in  it,  the  results  would 


LACTIC    ACID  41 

entirely  differ.  We  should  find  the  tissues  soft  and 
gelatinous,  and  instead  of  rigidity  we  should  find  the 
tissues  would  tend  to  break  up  as  we  handled  them. 

This  may  convey  the  idea  that  lactic  acid  had  a 
direct  destructive  action  on  animal  tissue  such  as  the 
stronger  inorganic  acids  possess.  But  if  we  look  at 
the  eye  of  the  fish  that  has  been  so  treated,  we  shall 
see  that  we  are  wrong  in  this  conclusion.  The  cornea 
remains  as  translucent  as  it  was  during  life.  We  know 
that  every  fibre  and  every  cell  has  been  invaded  by 
lactic  acid  in  large  quantities,  but  not  a  single  cell  has 
been  destroyed.  We  might  think  the  effects  were 
produced  by  coagulation,  as  is  always  suggested  to 
account  for  the  '  rigor  mortis ' ;  but  we  cannot  adopt 
that  view  and  account  for  the  transparency  of  the 
cornea ;  neither  does  it  help  us  to  explain  the  peculiar 
transparency  of  the  muscles  and  the  tissues  which 
takes  place  when  a  lactified  piece  of  animal  tissue  has 
been  exposed  to  the  air  for  some  time  ;  on  the  contrary, 
it  makes  the  theory  of  coagulation  impossible. 

I  have  not  described  the  actual  chemical  combinations 
which  lactic  acid  makes  with  the  tissues,  or  the  reason 
why  it  causes  rigidity  when  weak  solutions  are  used  and 
great  friability  of  the  tissues  when  we  employ  stronger 
solutions,  because  this  will  best  be  considered  in  the 
next  chapter. 


42 


CHAPTER    IV. 

THE    GENESIS    OF    THE    LITHATE. 

THE  concretions  found  in  and  around  the  joints  in 
patients  of  the  lithic  diathesis  are  practically  insoluble, 
and  occupy  fixed  positions  from  which  the  great  physical 
pressure  brought  to  bear  upon  them  during  the  use  of 
the  joints  fails  to  dislodge  them.  Now  the  urate,  as  we 
have  seen,  is  a  highly  soluble  body,  possessing  less  ten- 
dency to  concretion  than  most  salts.  It  moves  freely  in 
the  blood  and  the  excretions  of  the  body. 

My  imagination  has  never  been  equal  to  the  task  of 
finding  any  salt  of  urea  which  could  produce  an  insoluble 
body  such  as  we  find  in  the  joints.  This  is  my  reason 
for  using  the  word  '  lithate'  instead  of  '  urate '. 

The  chemists  have  made  two  urates  in  the  laboratory 
— an  acid  urate  or  biurate,  which  is  prepared  by  boiling 
an  alkaline  carbonate  with  uric  acid  ;  and  a  quadriurate, 
which  is  hyperacid  and  is  prepared  by  boiling  uric  acid 
with  dilute  solutions  of  acetate  of  potassium.  Of  these 
two  salts  the  biurate  is  the  less  soluble,  and  is  credited 
with  being  the  urate  deposited  in  the  joint.  But  clini- 
cally we  have  to  deal  with  a  concretion  which  remains  in 
the  tissues  for  months  or  years,  subject  to  all  the  solvent 
processes  of  the  body,  and  to  describe  this  as  consisting 
of  the  less  soluble  of  two  very  soluble  salts  has  always 
appeared  to  me  to  throw  a  great  strain  upon  our 
credulity. 

If  we  introduced  crystals  of  either  of  these  urates  into 
the  tissues  they  would  not  remain  there  for  five  minutes. 


THE    GENESIS    OF    THE    LIT H ATE  43 

Even  if  we  accepted  the  view  that  the  concretion  was  a 
urate,  and  through  some  mysterious  process  it  had 
become  insoluble,  we  should  still  have  to  account  for  its 
fixed  position  in  the  tissues.  We  should  have  to  endow 
the  crystal  with  the  capacities  of  a  limpet  in  order  to 
account  for  it. 

To  understand  the  lithate  we  must  go  back  to  the 
dead  cell.  When  I  stated  that  urea  was  the  ultimate 
product  of  the  cell,  I  referred  to  its  protoplasmic  con- 
tents. I  have  so  far  made  no  reference  to  the  wall  of 
the  cell,  which  is  constituted  differently  from  the  cell- 
contents,  and  therefore  its  katabolism  must  take  a 
different  form. 

Before  we  consider  this  point  it  is  necessary  that  we 
shall  have  a  clear  idea  of  the  nature  of  the  cell-wall. 
Kolliker  described  it  as  follows  :  "  The  membrane  of 
cells  is  mostly  very  delicate,  smooth,  scarcely  capable  of 
being  isolated,  and  bounded  by  simple  outlines,  more 
rarely  of  considerable  firmness  and  measurable  thick- 
ness. Amongst  the  latter,  we  must  include  the  cell- 
wall  of  the  cartilages  and  fibrous  tissue,  which  are 
thicker  than  those  of  other  tissues  ". 

But  if  we  accept  this  idea  of  the  cell-wall,  and  also 
that  all  tissues  are  built  up  of  cells,  how  are  we  going  to 
explain  the  great  tenacity  of  all  tissues  ?  How  do  the 
cells  that  build  up  a  tendon  hold  together  when  a  great 
strain  is  put  upon  it  during  physical  exertion  ?  We 
must  regard  the  cell-wall  not  merely  as  covering  to  the 
cell, '  resembling  fibrous  tissue ',  but  as  the  cement  which 
binds  them  together. 

Just  as  a  house  would  fall  to  pieces  during  the  first 
wind  which  blew  upon  it  except  for  the  mortar  which 
holds  the  bricks  in  place,  so  would  the  tissues  fall  to 
pieces  unless  their  cell  walls  acted  as  a  strong  cement 


44  THE    GENESIS    OF    THE    LITHATE 

to  hold  them  together.  Mortar  is  largely  composed  of 
lime,  and  nature  uses  the  same  substance  to  act  as  a 
cement  in  the  case  of  the  cell-wall. 

The  form  of  lime  used  is  the  phosphate,  and  the  affinity 
of  lactic  acid  for  lime  is  so  great  that  we  cannot  imagine 
phosphate  of  lime  to  exist  in  the  presence  of  lactic  acid 
without  combination  taking  place.  We  never  find 
phosphate  of  lime  in  the  body  except  in  combination 
with  lactic  acid.  If  we  dissolve  phosphate  of  lime  in 
lactic  acid  and  allow  a  drop  to  evaporate  on  a  glass 
slide,  we  shall  obtain  a  translucent  substance  which 
resembles  varnish,  and  has  the  same  adhesiveness  which 
a  varnish  possesses  when  it  is  nearly  dry.  It  is  what  the 
mechanic  calls  '  tacky ',  the  condition  in  which  he  likes 
the  glue  to  become  before  he  joins  two  pieces  of  wood 
together. 

When  I  described  the  great  affinity  which  lactic  acid 
had  for  animal  tissue,  it  was  really  the  attraction  exerted 
by  the  lime  in  the  cell-wall  which  was  referred  to.  It 
combines  with  this  lime  in  large  quantities  without  in 
any  way  injuring  or  invading  the  contents  01  the  cell. 
It  is  because  of  this  that  it  causes  no  destruction  of 
tissue. 

The  lime  of  the  cell-wall  serves  another  useful  purpose 
in  neutralizing  the  acidity  of  lactic  acid.  Like  ammonia, 
it  has  quite  remarkable  powers  as  an  antacid  in  rela- 
tion to  lactic  acid.  This  helps  us  further  to  understand 
the  way  in  which  nature  preserves  the  alkalinity  of  the 
tissues  and  the  blood. 

It  does  not  follow  that  all  the  lactic  acid  in  the 
cell-wall  is  in  chemical  combination  with  the  lime.  I 
have  demonstrated  by  experiment  that  the  cell-wall  is 
able  to  hold  very  large  quantities  of  lactic  acid,  and  in 
such  a  state  of  cohesion  that  the  acid  is  unable  to 


THE    GENESIS    OF    THE    LITHATE  45 

destroy  the  alkalinity  of  the  fluids  which  surround  it. 
We  are  sure  that  a  large  portion  of  this  lactic  acid  is 
held  by  simple  cohesion,  because  the  action  of  heat 
alone  is  able  to  liberate  it.  The  stiffness  and  rigidity 
of  tissues  produced  by  lactic  acid  appears  to  be  due 
to  a  mechanical  increase  in  the  thickness  of  the  cell- 
wall  due  to  its  presence.  The  cell-wall  must  swell 
owing  to  the  increase  in  its  contents,  and  there  is  no 
evidence  of  any  chemical  change  taking  place,  as  the 
excess  of  lactic  acid  can  again  be  liberated  by  the 
simple  action  of  heat.  We  can  now  understand  how 
it  is  that  urea  can  combine  with  sodium  chloride 
in  the  presence  of  lactic  acid.  The  lactic  acid  is 
locked  up  by  the  lime  in  the  walls  of  the  cell,  so  that 
the  chemical  reactions  of  the  protoplasm  within  the 
cell  are  not  interfered  with. 

We  also  can  better  realize  why  the  dead  epithelial  cell 
is  so  difficult  to  dislodge  in  the  absence  of  the  lactic 
acid  contained  in  the  sweat,  which  acts  as  a  solvent  to 
the  '  cement '  which  holds  it  there,  as  we  have  seen  in 
our  experiment  with  strong  lactic  acid  solution.  The 
tissues  become  friable  and  readily  fall  to  pieces,  because 
lactic  acid  has  dissolved  the  cement  which  holds  them 
together;  but  even  under  these  conditions,  lactic  acid 
has  not  invaded  the  cell  itself,  or  destroyed  it,  as  was 
made  evident  by  the  continued  transparency  of  the 
cornea  of  the  lactified  fish. 

Lactophosphate  of  lime  as  we  find  it  in  the  excretions 
is  a  perfectly  soluble  body.  It  appears  under  the 
microscope  as  round  or  oval  dark  bodies,  of  varying 
sizes,  the  smallest  being  larger  than  the  urate.  This  is 
how  it  appears  in  relation  to  other  bodies  in  the  field. 
But  if  we  change  the  focus  so  as  to  examine  the  struc- 
ture of  the  individual  body,  we  find  that  it  is  not  a  single 


46  THE    GENESIS    OF    THE    LITE  ATE 

crystal,  but  a  nest  of  very  minute  crystals  in  close 
cohesion.  Here  we  have  a  very  striking  difference 
between  the  urates  and  the  lime  salts.  The  urate 
always  appears  as  a  distinct  crystal,  keeping  a  space 
between  it  and  the  next  crystal.  If  we  concentrate 
the  solution  so  that  this  spacing  is  not  possible,  the 
urates  will  then  appear  each  as  distinct  as  pebbles 
on  the  sea-shore.  Lime,  on  the  other  hand,  never 
appears  except  in  small  concretions,  no  matter  how 
dilute  we  may  make  the  solution. 

No  amount  of  chemical  research  will  reveal  these 
physical  facts,  which  are  very  important  both  clinically 
and  physiologically. 

A  solution  of  lactophosphate  of  lime  can  be  made 
by  simply  dissolving  phosphate  of  lime  in  lactic  acid. 
I  have  also  prepared  it  by  boiling  the  tendons  of 
animals  in  lactic  acid.  On  comparing  the  crystals  of 
both  these  solutions  with  the  crystals  of  lactophosphate 
of  lime  which  one  meets  with  in  abundance  in  the  sweat 
of  rheumatic  patients,  I  find  them  identical,  not  only  in 
form,  but  also  in  the  peculiar  characteristics  I  shall  now 
describe. 

If  we  evaporate  a  drop  of  lactophosphate  of  lime 
on  a  glass  slide,  it  has  the  appearance  I  have  already 
mentioned  (Plate  III,  Fig.  8). 

If  we  leave  it  for  twenty-four  hours  we  shall  find  it 
has  begun  to  sprout  like  a  seed  germinating,  only  in- 
stead of  a  single  sprout  there  are  a  number,  because 
each  little  crystal  in  the  mass  is,  as  it  were,  germinating. 
We  thus  get  the  peculiar  bodies  which  are  illustrated  in 
Plate  III,  Fig.  9,  and  at  a  later  stage  the  condition 
shown  in  Plate  III,  Fig.  10. 

If  we  keep  the  preparation  for  some  days,  we  shall 
find  that  each  of  these  little  sprouts  develops  into  a  rod- 


PLATE    III. 


Fig.  8 


fig:  <?• 


Fig.  10. 


PLATE     IV. 


Fig    n. 


fig. 


THE    GENESIS    OF    THE    LIT  HATE  47 

like  structure,  and  as  these  are  pushed  out  from  a  com- 
mon centre,  the  result  is  that  we  get  a  central  nucleus 
with  rays  in  all  directions  like  the  spokes  of  a  wheel. 
Or  we  may  have  these  rods  only  at  two  ends  of  the 
central  nucleus,  so  that  it  looks  like  a  bundle  of  sticks 
tied  at  the  centre  (Plate  IV,  Fig  n).  Finally  the  rods 
break  off  from  the  central  nucleus  and  appear  as  in 
Plate  IV,  Fig.  12,  and  become  gradually  shorter  as 
oxidation  progresses.* 

Hydrate  of  lime  goes  through  the  same  transform- 
ation, but  instead  of  the  rods  being  straight  like  sticks, 
they  branch  as  they  grow,  and  the  branches  can  be 
carried  to  a  great  length  from  the  original  crystal. 
This  will  explain  the  remarkable  binding  properties 
of  lime  ;  not  only  have  its  owrn  particles  a  great  tend- 
ency to  cohesion,  but  by  their  branches  they  can  bind 
together  any  other  matter  which  may  exist  in  the  mass 
(Plate  V,  Fig.  13). 

During  this  process  the  solubility  of  the  phosphate  of 
lime  steadily  diminishes,  so  that  without  other  influence 
than  the  air  to  which  the  drop  of  lactophosphate  of 
lime  was  exposed  we  can  see  a  soluble  body  becoming 
almost  insoluble.  We  see,  therefore,  that  the  normal 
constituents  of  the  cell-wall  provide  us  with  all  the 
material  for  the  manufacture  of  the  lithate.  It  is 
wholly  unnecessary  for  us  to  imagine  that  the  blood 
brings  it  there  and  deposits  it. 

*These  plates  are  made  from  negatives  taken  on  paper.  They 
are  therefore  complete  as  soon  as  developed.  This  method 
saves  a  great  amount  of  time  when  a  large  number  of  micro- 
photos  have  to  be  made.  The  difficulty  is  to  secure  a  suitable 
paper.  The  Imperial  Dry  Plate  Co.,  of  Cricklewood,  London, 
N.W.2,  have  made  a  large  number  of  experiments  on  this  point, 
and  at  last  were  able  to  supply  me  with  a  very  rapid  paper. 
I  am  much  indebted  to  them  for  the  great  trouble  taken  to 
assist  me. 


48  THE    GENESIS    OF    THE    LITHATE 

But  the  reader  will  very  naturally  say  that  the 
-deposits  found  in  the  joints  of  patients  with  gout  have 
been  proved  to  consist  of  '  urate  of  soda  ',  and  this  has 
been  confirmed  by  chemical  analysis.  I  will  leave  the 
chemical  part  of  the  question  until  the  next  chapter ; 
here  we  are  most  concerned  with  the  physical  properties 
and  microscopic  appearances  of  these  deposits. 

Garrod,  in  his  work  on  Gout  and  Rheumatic  Gout, 
furnishes  us  with  some  excellent  illustrations  of  the 
crystals  which  he  found  in  the  joints,  and  to  which  he 
gave  the  name  of  urate  of  soda.  Plate  V,  Fig.  14  shows 
crystals  in  the  stellate  form  which  it  would  be  impossible 
to  reproduce  by  any  combination  of  urea,  and  which  are 
characteristic  of  the  formation  of  lactophosphate  of 
lime  in  a  certain  stage  of  oxidation.  In  the  same 
illustration  we  find  the  tiny  rods  which  occur  when  a 
higher  state  of  oxidation  has  been  reached. 

He  also  gives  us  another  illustration  which  he 
describes  as  urate  of  soda,  in  which  we  see  the  stellate 
crystals  of  lactophosphate  of  lime  after  the  rods  have 
broken  off  (Plate  V,  Fig.  15). 

Garrod  was  not  alone  in  making  this  remarkable 
histological  mistake.  Thus,  in  Golding  Bird's  classical 
work  on  urinary  deposits  I  find  some  excellent  illustra- 
tions of  lactophosphate  of  lime  in  its  various  stages 
of  oxidation  described  as  'urate  of  soda'.  Fig.  16 
represents  the  nest  of  crystals  as  they  are  commencing 
to  sprout  ;  Fig.  17  shows  the  same  in  an  advanced 
stage  of  oxidation. 

It  is  only  necessary  to  compare  these  illustrations 
with  the  photographs  I  have  made  of  lactophosphate 
of  lime  in  its  various  stages  to  recognize  the  mistake 
that  has  been  made.  There  can  be  no  question  of  a 
similarity  between  the  crystals,  because  urate  of  soda 


PLATE     V. 


'3- 


.  14 


Fig.  Ij 


PLATE     V. 


fig-  13- 


fig.  14. 


F'S- 


THE    GENESIS    OF    THE    LIT  HATE 


49 


does  not  exist  in  the  body,  and  cannot  do  so,  for  reasons 
I  shall  presently  explain. 

From  what  I  have  already  described  about  the  remark- 
able tenacity  of  the  dead  cell  to  the  living  cell,  we  have 
sufficient  explanation  of  why  these  concretions  remain 
constant  in  the  tissues,  in  spite  of  all  the  forces  brought 
to  bear  upon  them.  It  remains  for  us  to  explain  the 
physical  causes  which  lead  to  these  deposits  being  formed, 
instead  of  the  lactophosphate  of  lime  disappearing  as  a 
soluble  salt  as  it  does  normally. 

It  will  be  remembered  that  these  concretions  only 


Fig.  ft). 


Fig:.  17- 


occur  in  the  fibrous  and  cartilaginous  tissue?,  never 
in  the  muscles  or  the  other  parts  of  the  body.  Now 
these  tissues,  which  are  the  site  of  the  deposits  of 
lithates,  occupy  a  position  in  the  body  which  is 
practically  outside  the  sphere  of  the  normal  circula- 
tion. If  we  make  a-s^ction  of  a  limb,  we  shall  find 
in  the  centre  the  bone,  which  has  a  proper  vascular 
supply  ;  next  we  shall  find  the  large  mass  of  muscles, 
with  their  own  circulation,  which  enables  them  to 
become  the  site  of  the  great  oxidizing  processes  of 
the  body.  At  the  circumference  of  the  section  we  have 
the  skin,  with  its  rich  capillary  circulation,  with  ducts 

4 


50  THE    GENESIS    OF    THE    LITHATE 

where  important  oxidizing  processes  are  carried  out. 
Between  the  skin  and  the  muscles  is  a  space,  and  the 
tissues  in  this  space  have  practically  no  circulation  of 
their  own,  but  are  dependent  upon  the  lymph  exuded 
from  its  walls  for  their  nutriment.  It  is  within  this 
great  lymph-space  that  we  find  the  tissues  in  which 
the  lithate  forms,  and  it  is  also  the  place  where  the 
metabolism  of  the  products  of  the  tissues  takes  place. 
The  chemical  changes  occurring  there  are  little  influenced 
by  the  processes  taking  place  in  the  far-away  alimentary 
canal,  less  than  would  be  supposed  by  the  active  circula- 
tion in  the  blood-vessels  immediately  outside  its  walls. 
The  conditions  which  effect  the  chemical  changes  are 
almost  entirely  physical,  and,  because  these  physical 
agencies  are  necessary  to  perfect  metabolism,  the  site 
selected  for  them  is  near  the  surface  of  the  body  and 
covers  the  whole  area  beneath  that  surface. 

An  internal  organ,  such  as  the  liver,  would  lack  all 
the  essential  conditions  necessary  to  the  processes  which 
take  place. 

What  happens  in  the  lymph-space  is  easily  intelligible. 
When  the  body  is  at  rest,  and  the  temperature  normal, 
there  is  a  slow  exudation  of  lymph  into  the  space,  which 
nourishes  the  tissues  within  and  supplies  the  necessary 
moisture  for  the  performance  of  their  functions.  Very 
little  lactic  acid  can  pass  into  the  space,  because  the 
muscles  are  inactive.  The  lymph,  having  performed  its 
functions  and  taken  up  some  of  the  products  of  kata- 
bolism,  becomes  itself  a  '  waste '  product,  and  has  to  be 
eliminated.  It  finds  its  way  by  the  lymphatics  through 
a  long  and  tortuous  course  to  the  thoracic  duct,  enters 
the  venous  circulation,  and  is  finally  eliminated  by  the 
kidney.  If  we  now  raise  the  temperature  of  the  body 
while  it  is  still  in  a  state  of  rest,  we  dilate  the  capillary 


THE    GENESIS    OF    THE    LITHATE  51 

walls  of  the  space,  and  allow  a  much  larger  influx 
of  lymph,  which  floods  the  space  and  brings  greater 
nourishment  to  the  tissues. 

The  body  being  at  rest  during  the  influx  of  lymph, 
there  is  no  increase  in  the  formation  of  lactic  acid  and 
its  excretion  into  the  space,  but  some  of  the  additive 
lactic  acid  locked  up  in  the  lactophosphate  of  lime  is  set 
free.  We  have  seen  this  happen  in  the  experiments  I 
have  described. 

The  effect  of  heat  on  the  body  is  to  fill  up  the 
lymph-space  with  fluid  and  set  lactic  acid  free;  but 
this  has  an  embarrassing  effect  upon  the  slow- 
moving  lymphatics,  which  find  themselves  unequal  to 
the  work  of  eliminating  the  fluid  as  fast  as  it  is  poured 
into  the  spaces.  This  difficulty  makes  itself  evident  to 
the  individual,  who  is  conscious  of  the  congested  con- 
dition which  results.  But  nature  has  made  proper 
arrangements  for  the  relief  of  this  condition.  The  fluid 
and  the  lactic  acid  stimulate  the  functions  of  the 
sweat-ducts,  which  eliminate  this  excess  of  fluid,  and 
immediate  relief  is  obtained. 

If  we  now  consider  the  conditions  produced  by  active 
exercise  of  the  muscles,  we  shall  find  all  the  factors 
present  which  existed  as  a  result  of  raising  the  tem- 
perature, but  we  shall  in  addition  have  a  large  accession 
of  lactic  acid  owing  to  the  activity  of  the  muscle. 

This  free  lactic  acid,  whether  produced  by  heat  or 
exercise,  has  a  valuable  effect  in  dissolving  the  cement 
which  causes  the  debris  of  the  dead  cell  to  remain  in 
contact  with  the  living  cell — because  the  cell  is  dead, 
lactic  acid  can  produce  its  solvent  influence.  But  the 
result  of  all  this  is  that  the  lymph-space  becomes 
crowded  with  fluid  containing  waste  products,  which 
must  be  quickly  eliminated,  or  prejudicial  effects  will  be 


52  THE    GENESIS    OF    THE    LITHATE 

produced  by  the  various  chemical  combinations  which 
must  take  place. 

Here,  again,  the  skin  by  its  excretion  comes  to  our 
aid.  The  same  causes  which  fill  up  the  lymph-space 
with  products  requiring  excretion,  increase  the  ex- 
cretory powers  of  the  skin.  The  great  result  then  of 
exercise  is  that  the  lymph-space  has  been  flushed 
with  fluid,  more  nourishment  has  been  brought  to  the 
tissues,  and  waste  products  have  been  eliminated. 

The  whole  scheme  of  nature  is  that  the  metabolism  in 
the  tissues  shall  have  its  periods  of  quiescence  and  its 
periods  of  activity,  and  that  there  should  be  those 
periodic  flushings  of  the  tissues  in  the  lymph-space,  just 
as  we  find  them  necessary  for  all  purposes  of  cleanliness. 

Under  these  conditions  the  lactophosphate  of  lime  of 
the  cell- wall  passes  away  as  a  highly  soluble  salt,  and 
is  so  unobtrusive  that  its  existence  has  hardly  been 
recognized. 

But  I  commenced  this  book  by  recording  observations 
upon  a  large  number  of  healthy  people  where  I  found 
evidence  of  lithates  in  or  around  their  joints,  of  which 
they  were  unconscious.  These  lithates  indicated  that 
they  had  collections  of  dead  cells  still  attached  to  the 
living  cells,  and  which  had  undergone  partial  oxidation 
so  as  to  become  nearly  insoluble. 

There  was  evidently  something  wrong  with  their 
physiological  processes,  although  they  were  apparently 
in  perfect  health,  took  exercise,  and  made  no  errors  in 
diet  which  I  could  discover.  But  I  found  that  these 
individuals  had  two  marked  peculiarities :  one  was  a  dry 
skin  that  did  not  easily  sweat  either  from  heat  or  by 
exercise,  and  the  other  was  a  persistent  subnormal 
temperature.  Both  these  conditions  may  exist  in 
persons  in  apparently  robust  health  and  who  are 

fi^J  !  ':<*    10    3fJ3JJ 
;- IJ  -.    ir.    ZKI  J  SlfcYU'i 
?.  .  f  J  .  ?  =  j  2  s  i'  /    ?  r,  j 


THE    GENESIS    OF    THE    LITHATE  53 

capable  of  great  physical  exertion.  The  conditions  for 
producing  lactic  acid  are  the  same  in  these  persons  as 
in  others,  but  the  power  to  eliminate  it  is  deficient. 

We  have  to  consider  what  happens  when  lactic  acid 
is  thrown  into  the  lymph-space  and  is  not  readily 
eliminated.  We  have  seen  from  the  experiments  I  have 
described  that  lactic  acid  has  a  very  strong  affinity  for 
the  cell-walls  of  the  tissues,  and  if  it  is  not  eliminated 
will  quickly  combine  with  them  instead  of  passing  away 
with  the  lymph  through  the  lymphatics. 

Lactophosphate  of  lime  as  we  find  it  in  the  lymph, 
the  sweat,  and  the  urine,  is  a  very  soluble  salt,  but  it 
is  soluble  because  there  is  sufficient  lactic  acid  present 
to  hold  the  lime  in  solution.  Lactophosphate  of  lime 
as  it  exists  in  the  normal  cell-wall  is  not  soluble,  neither 
is  it  when  we  find  it  as  lithate  in  the  tissues.  But  the 
question  of  the  decreased  solubility  of  the  salt  is  not 
wholly  dependent  upon  its  lactic-acid  content.  We 
have  seen  that  the  soluble  salt  'becomes  less  soluble 
when  exposed  to  the  air,  under  the  influence  of  oxygen. 
If  we  expose  it  to  the  action  of  sulphuric  acid,  which  is 
at  once  an  acid  and  an  oxidizing  agent,  sparingly 
soluble  crystals  are  at  once  formed.  But,  in  spite  of 
this  fact,  it  attains  its  greatest  insolubility  under  the 
influence  of  ammonia,  which  precipitates  it  from  its 
solution.  Therefore  we  are  under  no  difficulties  in 
explaining  the  presence  of  an  insoluble  lactophosphate 
of  lime  in  the  body,  as  we  are  if  we  try  to  represent 
the  insoluble  substance  found  as  a  urate. 

That  these  lithates  are  characteristic  of  '  gout '  can 
well  be  understood,  because,  as  we  shall  see,  there 
is  not  only  a  diminished  production  of  lactic  acid,  but 
also  there  are  conditions  which  cause  the  lactic  acid  to 
be  locked  up  as  lactate  of  ammonia. 


54  THE    GENESIS    OF    THE    LITHATE 

But  we  should  imagine  that  the  presence  of  lactic 
acid  would  assist  the  detachment  of  the  dead  cell  from 
the  living  cell.  It  does  so  under  certain  conditions.  If 
the  patient  with  a  functionally  inactive  skin  takes  plenty 
of  exercise  and  the  body  is  kept  warm,  his  lymph -space 
will  be  flushed  with  fluid  containing  lactic  acid.  This 
will  dissolve  up  the  debris  of  the  cell-wall,  and  he  will 
produce  a  quantity  of  lactophosphate  of  lime  in  a  sol- 
uble form.  But  this  has  to  be  excreted,  and,  as  the  skin 
does  not  act,  the  whole  work  is  thrown  upon  the  lymph- 
atics and,  finally,  the  kidney.  The  result  is  that  one  of 
the  most  noted  symptoms  of  '  gout '  is  that  the  patient 
passes  large  quantities  of  lithates  in  the  urine,  he  may 
have  gravel  or  stone  in  the  kidney,  and  as  an  end-result 
the  kidneys  themselves  become  impaired.  Some  writers 
on  gout  have  regarded  this  impairment  of  the  kidneys 
as  a  cause  of  gout,  instead  of  one  of  the  final  results  of 
years  of  overwork  and  undue  irritation. 

When  we  find  lithates  in  the  joints  of  these  patients, 
it  will  be  usually  in  the  great-toe-joint,  or  the  shoulder, 
because  neither  of  these  joints  gets  that  amount  of 
exercise  which  is  necessary  to  maintain  it  in  normal 
physiological  activity.  Or  we  may  find  the  urates  in 
some  joint  which  has  at  one  time  been  injured,  although 
the  injury  itself  has  been  long  ago  forgotten,  but  the 
tissues  have  not  recovered  their  full  activity. 

We  shall  find  the  lithates  more  abundant  in  the  joints 
of  those  who,  having  a  skin  with  defective  functional 
power,  take  very  little  exercise,  and  so  do  not  produce 
a  sufficiency  of  lactic  acid  to  dissolve  the  lactophosphate 
of  lime.  In  these  cases  we  shall  not  find  the  same 
tendency  to  pass  lithates  in  the  urine,  because  there  is 
little  to  pass.  The  lactic  acid  which  is  formed  combines 
with  the  lime  in  the  tissues,  and  therefore  we  find  in 


THE    GENESIS    OF    THE    LITHATE  55 

such  patients  a  large  amount  of  lactic  acid  locked  up 
in  the  tissues,  so  that  its  normal  work  is  not  performed. 
This  fact  can  be  demonstrated  by  the  effect  of  the  daily 
administration  of  baths  which  raise  the  temperature 
of  the  body.  The  lactic  acid  is  slowly  liberated,  and 
the  reaction  of  the  skin  shows  a  steady  increase  in 
its  acidity. 

We  have  to  remember  in  these  cases  that  the  tempera- 
ture of  the  patient  is  subnormal,  and  the  active  exercise, 
which  might  produce  a  temporary  rise,  is  absent  from 
the  daily  routine.  Consequently,  the  lymph  poured  into 
the  tissues  is  deficient,  and  there  is  not  a  sufficient 
surplus  to  act  as  a  solvent,  so  the  dead  cell,  slowly 
undergoing  oxidation,  remains  in  contact  with  the  living 
cell,  and  presently  we  recognize  its  existence  by  finding 
crepitation  in  the  joints. 

Next  to  the  failure  of  the  action  of  the  skin,  cold  and 
diminished  temperature  of  the  body  are  the  most  potent 
agents  in  the  production  of  the  lithates  in  the  joints. 
Cold  contracts  the  capillary  blood-vessels  and  dimin- 
ishes the  flow  of  lymph,  and  the  lymph-space  becomes 
muddy  from  undissolved  excretion. 


56 


CHAPTER    V. 

THE    GENESIS    OF    URIC    ACID. 

TOWARDS  the  end  of  the  eighteenth  century,  Murray 
Forbes,  observing  the  connection  between  gout  and 
gravel,  and  the  tendency  of  the  gouty  patient  to  form 
concretions,  ascribed  it  to  lithiasic  or  lithic  acid  in  the 
blood.  In  1848  Garrod  described  his  well-known 
experiment.  He  added  acetic  acid  to  lymph,  put  it  in 
a  warm  place  for  about  forty-eight  hours,  and  then 
found  uric  acid  adhering  to  a  piece  of  thread  which  he 
had  placed  in  the  solution. 

This  experiment  proves  that  when  lymph  undergoes 
decomposition  in  an  acid  solution,  it  is  capable  of  yield- 
ing uric  acid.  We  know  that  when  the  constituents  of 
lymph  reach  the  kidney  and  undergo  decomposition  in 
an  acid  solution,  they  may  produce  uric  acid,  abnor- 
mally in  man,  but  normally  in  birds.  But  Garrod 
asserted  that  he  had  found  uric  acid  in  the  blood,  and 
also  that  he  had  found  it  in  the  form  of  urate  of  soda. 
Garrod  found,  from  a  concentrated  watery  solution 
obtained  from  lymph  and  allowed  to  stand  for  some 
hours,  numerous  tufts  of  crystals,  deposited  on  the 
sides  of  the  vessel.  He  found  that  on  the  addition  of 
hydrochloric  acid  they  yielded  rhombs  of  uric  acid. 
When  these  crystals  were  incinerated  they  left  an  ash, 
alkaline  in  reaction,  soluble  in  water,  which  did  not 
answer  to  the  tests  for  potash.  He  therefore  pro- 
nounced them  to  be  urate  of  soda  (Gout  and  Rheumatic 
Gout,  p.  98). 


THE    GENESIS    OF    URIC    ACID  57 

Neither  Garrod  nor  any  observer  since  has  actually 
demonstrated  the  presence  of  urate  of  soda  in  the 
blood,  but  it  has  become  universally  accepted,  and 
the  uric-acid  theory  of  gout  is  based  upon  it.  From 
the  descriptions  in  text-books  it  would  appear  as  if 
urate  of  soda  were  simply  the  union  of  an  acid  with  a 
base.  Uric  acid  is  really  a  very  complex  body,  and 
has  no  affinity  for  soda. 

If  we  place  uric  acid  in  a  solution  of  carbonate  of 
soda  and  maintain  the  solution  at  blood  heat  for  a 
considerable  time,  no  combination  takes  place ;  neither 
does  the  uric  acid  dissolve  in  the  carbonate  of  soda, 
although  we  are  always  taught  that  carbonate  of  soda 
is  a  solvent  of  uric  acid.  It  is  not  until  the  solution 
is  boiled  for  some  time  that  solution  and  combination 
take  place. 

Writers  on  gout  tell  us  that  uric  acid  is  formed  in  the 
liver  and  immediately  combines  with  soda  to  form  urate 
of  soda;  some  of  this  is  carried  to  the  kidney  and 
some  finds  its  way  to  the  blood.  Nature  possesses  no 
arrangement  for  boiling  uric  acid,  and  any  delay  in 
the  combination  would  certainly  result  in  uric-acid 
calculus  in  the  liver,  a  disorder  which  fortunately  never 
occurs. 

The  ordinary  method  of  demonstrating  the  presence 
of  uric  acid  in  urine  is  practically  the  same  as  Garrod's 
test.  A  strong  acid,  usually  hydrochloric,  is  added  to 
urine.  Now,  as  the  urine  is  supposed  to  contain  urate 
of  soda,  and  uric  acid  is  a  weak  acid,  one  might  suppose 
that  the  strong  acid  would  combine  with  the  soda  and 
the  uric  acid  would  be  thrown  out  of  solution ;  but  this 
result  does  not  happen.  The  addition  of  a  strong  acid 
to  normal  urine  produces  no  visible  effect.  We  must 
put  it  away  in  a  warm  place  for  twenty-four  to  forty- 


58  THE    GENESIS    OF    URIC    ACID 

eight  hours,  and  then  if  we  are  lucky — for  the  experiment 
frequently  fails — we  shall  find  some  uric  acid  at  the 
bottom  of  the  test-tube.  The  chemical  change  which 
actually  takes  place  from  the  addition  of  the  acid  will 
best  be  explained  when  we  have  considered  the  following 
further  method  of  demonstrating  the  presence  of  uric 
acid  in  urine. 

The  urine  is  saturated  with  chloride  of  ammonium, 
and  then  a  few  drops  of  liq.  ammoniae  fort,  are  added. 
There  is  usually  a  very  dense  gelatinous  precipitate, 
which  is  called  urate  of  ammonium,  and  which  has  been 
given  the  formula  CfiN4H3NH4O3. 

This  salt  is  of  very  great  clinical  importance,  because 
it  is  used  in  the  experiments  by  which  the  exact  quantity 
of  uric  acid  in  the  urine  is  determined. 

From  the  results  of  these  experiments  we  derive  our 
knowledge  respecting  the  influence  of  foods  upon  the 
excretion  of  uric  acid.  What  is  called  the  '  titration 
method'  is  used,  and  is  based  upon  the  oxidizing 
power  of  urate  of  ammonium  on  a  standard  solution  of 
permanganate  of  potash. 

"  The  urine  is  titrated  with  colloidal  iron  to  remove 
an  unknown  substance  that  is  precipitated  by  am- 
monium chloride,  and  made  strongly  alkaline  with 
ammonia.  The  uric  acid  is  rapidly  and  quantitatively 
precipitated  as  ammonium  urate.  This  is  filtered  off, 
washed  with  ammonium  sulphate  to  remove  the  greater 
part  of  the  chlorides,  dissolved  in  hot  sulphuric  acid, 
and  titrated  with  standard  potassium  permanganate. 
The  end  point  is  reached  when  a  momentary  pink  flush 
is  seen  over  the  whole  body  of  the  fluid."  (S.  W.  Cole, 
Practical  Physiological  Chemistry,  p.  341.) 

In  this  experiment  it  is  taken  for  granted  that 
ammonia  and  chloride  of  ammonium  have  the  property 


THE    GENESIS    OF    URIC    ACID  59 

of  precipitating  urates  from  solution.  If  we  saturate 
a  solution  of  urea  with  chloride  of  ammonium,  and 
then  add  ammonia,  we  obtain  no  precipitate. 

If  we  perform  the  same  experiment  with  a  solution 
of  urate  of  sodium  (i.e.,  uric  acid  dissolved  in  carbonate 
of  soda),  no  precipitate  falls.  There  is  nothing  to 
suggest  that  ammonia  (NHL)  would  have  the  property 
of  forming  an  insoluble  compound  with  urea  or  any 
salt  of  uric  acid.  Yet  it  is  universally  accepted  that  it 
does  so.  We  know  that  chloride  of  ammonium  and 
ammonia  are  the  reagents  used  by  chemists  to  pre- 
cipitate the  phosphate  of  lime  and  magnesia  from 
solution,  and  the  urine  contains  both  these  ingredients. 
If  we  use  these  reagents  to  an  ordinary  solution  of 
sulphate  of  magnesia,  we  shall  cause  a  white  precipitate. 
Now  it  is  absolutely  impossible  to  add  these  ingredients 
to  normal  urine  without  causing  a  precipitate  of  lacto- 
phosphate  of  lime ;  it  is  also  equally  impossible  to 
precipitate  urea,  or  any  salt  of  uric  acid,  with  these 
reagents. 

The  answer  to  this  objection  is  that  the  chemist 
can  produce  uric  acid  by  adding  an  acid  to  this  pre- 
cipitate ;  but  the  inference  that  this  is  a  proof  that 
the  precipitate  therefore  contained  uric  acid  is  open  to 
serious  question. 

Chemically  we  have  no  proof  that  the  precipitate 
contained  any  nitrogenous  product  whatever,  beyond 
the  ammonia  which  the  chemist  has  himself  added  ; 
and  while  this  ammonia  may  be  used  for  the  synthesis 
of  uric  acid,  it  cannot  precipitate  uric  acid  already 
formed  from  solution. 

To  make  myself  clear  upon  this  point,  I  added  chloride 
of  ammonia  and  liq.  ammonise  fort,  to  a  specimen  of 
urine,  and  produced  the  gelatinous  precipitate  called 


60 


THE    GENESIS    OF    URIC    ACID 


'  urate  of  ammonia '.  I  used  the  same  ingredients  in 
exactly  the  same  way,  to  a  solution  of  lactophosphate 
of  lime,  and  produced  a  gelatinous  precipitate.  I 


Fig.  /8. 


dissolved  each  precipitate  in  dilute  sulphuric  acid  and 
examined  them  microscopically.  The  result  is  shown  in 
the  accompanying  illustrations.  Fig.  18  represents  the 


Fig.  Jp. 


precipitate   obtained    from   urine,    and   Fig.    19    that 
obtained  from  lactophosphate  of  lime. 

In  the  former  illustration  there  are  some  granular 


THE    GENESIS    OF    URIC    ACID  61 

particles  which  do  not  appear  in  the  second.  The 
precipitate  obtained  from  urine  by  these  reagents  con- 
tains some  of  the  colouring  matter  of  the  urine ;  and  as 
this  enters  into  the  composition  of  the  uric-acid  crystal, 
and  appears  to  be  an  essential  part  of  it,  the  fact  is  of 
importance.  The  crystals  I  have  illustrated  above,  due 
to  the  action  of  sulphuric  acid  on  lactophosphate  of 
lime,  were  noticed  and  illustrated  by  Golding  Bird  in 
his  work  on  urinary  deposits,  and  were  described  by 
him  as  '  urate  of  soda  '  (Fig.  20) . 

To  revert  to  the  '  titration  method ',  the  final  result, 


Fig.  20. 

by  which  the  amount  of  uric  acid  is  determined,  is 
obtained  by  dropping  a  standard  solution  of  perman- 
ganate of  potash  into  the  solution,  and  there  comes  a 
moment  when  the  colour  does  not  disappear  and  a  pink 
flush  is  seen  in  the  fluid.  But  if  we  perform  the  same 
experiment  with  a  solution  of  lactophosphate  of  lime, 
we  shall  obtain  the  same  results.  If  uric  acid  actually 
existed  in  the  solution,  we  should  not  expect  the 
reaction,  because  it  is  a  stable  body  and  has  not  the 
chemical  activity  or  oxidizing  power  of  phosphate  of  lime. 
It  will  be  noticed  that,  throughout  this  inquiry,  when 
we  think  we  have  come  upon  uric  acid,  or  urates,  we 


62  THE    GENESIS    OF    URIC    ACID 

invariably  find  ourselves  in  contact  with  lactophosphate 
of  lime.  For  convenience  I  have  prepared  a  diagram 
showing  the  changes  which  lactophosphate  of  lime 
undergoes  when  simply  exposed  to  the  air.  As  I  have 
already  shown,  each  of  these  varied  forms  has  been 
described  by  one  observer  or  another  as  '  urate  of  soda  '. 
They  have  done  so  because  they  found  that  by  add- 
ing an  acid  they  could  produce  the  rhomboid  crystals 
known  as  '  uric  acid  '.  (See  Fig.  2j.} 

I  have  alluded  to  Garrod's  experiment.  He  dis- 
covered tufts  of  crystals  in  a  concentrated  watery 
solution  obtained  from  lymph,  and  he  found  that  when 
they  were  incinerated  "  they  left  an  ash,  alkaline  in 
reaction,  which  did  not  answer  to  the  tests  for  potash", 
and  therefore  he  concluded  that  it  was  soda.  It  did  not 
occur  to  him  that  it  was  lime,  and  that  what  he  called 
urate  of  soda  was  really  lactophosphate  of  lime. 

But  now  we  come  to  a  difficult  problem.  How  does 
it  happen  that  lactophosphate  of  lime  in  the  presence 
of  a  strong  acid,  and  after  exposure  to  the  air,  yields 
'  uric  acid  '  ? 

We  have  to  remember  that  in  all  these  experiments 
we  are  not  dealing  with  a  pure  solution  of  lactophosphate 
of  lime,  but  with  a  solution  originally  containing  urea, 
which  becomes  converted  into  ammonia  during  the 
experiment,  or  with  ammonia  directly  added  by  the 
chemist. 

Thus,  when  Garrod  "  discovered  uric  acid  in  the 
blood  ",  he  made  the  lymph  strongly  acid,  and  then 
left  the  lymph  to  decompose  in  a  warm  place  for  thirty- 
six  hours  or  longer.  The  result  was  that  the  urea 
became  converted  into  ammonia,  and  this  in  its  free 
state  has  the  property  of  precipitating  lactophosphate 
of  lime. 


THE    GENESIS    OF    URIC    ACID  63 


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64  THE    GENESIS    OF    URIC    ACID 

In  the  titration  test  we  do  not  wait  to  manufacture 
ammonia  from  urea,  but  saturate  the  urine  with  chloride 
of  ammonium,  and  then  add  some  ammonia,  and  having 
precipitated  the  lactophosphates  we  redissolve  them 
with  hydrochloric  acid.  This  all  points  to  uric  acid 
being  formed  by  some  reaction  which  takes  place 
between  lactophosphate  of  lime  and  ammonia  in  the 
presence  of  an  acid  and  oxygen.  It  would  appear 
from  this  that  the  synthesis  of  uric  acid  would  be  a 
very  simple  matter. 

Not  being  a  chemist,  I  have  found  it  a  very  difficult 
problem,  one  of  the  difficulties  being  that  the  so-called 
urate  of  ammonium  contains  some  of  the  colouring 
matter  of  the  urine,  and  is  not  a  simple  compound  of 
ammonia  and  lactophosphate  of  lime. 

But  the  genesis  of  uric  acid  can  be  rendered  intelligible 
from  the  following  experiments. 

We  have  seen  that  when  lactophosphate  of  lime  is 
exposed  to  the  air  for  a  prolonged  period,  it  finally 
forms  very  small  fine  rods  (see  Fig.  26).  If  we 
add  an  excess  of  lactic  acid  to  the  solution,  and  then 
place  a  drop  on  a  glass  slide  and  add  to  it  two  drops 
of  peroxide  of  hydrogen  (20  vols.},  the  excess  of 
lactic  acid  prevents  evaporation.  In  about  six  hours 
we  shall  notice  crystals  being  thrown  out  of  solution, 
and  these  crystals  are  identical  in  form  with  those 
of  uric  acid — not  only  do  we  find  the  ordinary 
rhombs,  but  in  varied  experiments  we  obtain  many  of 
the  less  common  forms  of  uric  acid  (see  Fig.  27). 
Now  it  is  a  little  difficult  to  understand  the  composition 
of  these  crystals.  Uric  acid  does  not  contain  either 
phosphoric  acid  or  lime,  but  it  does  contain  nitrogen. 
In  this  solution  we  have  no  nitrogen  unless  it  has 
absorbed  ammonia  from  the  air;  yet  these  crystals 


THE    GENESIS    OF    URIC    ACID  65 

are  identical  in  form  with  uric  acid,  although  they  do 
not  possess  its  insolubility. 

The  chemical  problem  can  best  be  understood  if  we 
consider  the  solution  in  which  chloride  of  ammonium 
is  combined  with  lactophosphate  of  lime  and  then 
exposed  to  the  influence  of  oxygen  and  an  acid.  When 
iactic  acid  is  oxidized  it  is  converted  into  carbonic  acid 
gas,  and  this  has  a  great  affinity  for  lime.  One  of  the 
first  stages,  therefore,  would  be  the  formation  of  car- 
bonate of  lime ;  but,  as  the  solution  is  highly  acid,  this 
would  be  at  once  converted  into  the  acid  carbonate 
of  iime,  which  has  no  tendency  to  crystallize.  But  the 
acid  carbonate  possesses  the  property  of  liberating 
ammonia  from  the  chloride  of  ammonia,  and  we  shall 
obtain  both  free  ammonia  and  carbonate  of  ammonia 
in  the  solution.  Now  as  a  result  of  these  chemical 
changes  phosphoric  acid  must  be  set  free,  and  as  it  is 
a  very  powerful  oxidizing  agent,  containing  as  it  does 
four  atoms  of  oxygen,  its  effect  upon  the  lactic  acid 
would  be  to  convert  some  of  it  into  carbonic  acid  gas  ; 
but  the  conversion  is  not  complete,  because  some  lactic 
acid  remains  in  the  solution  and  forms  a  lactocarbonate 
of  ammonium.  It  will  be  thus  seen  that  although 
lactophosphate  of  lime  is  essential  to  the  chemical 
changes  brought  about,  it  forms  no  part  of  the  final 
product. 

That  these  results  are  not  purely  theoretical  can  be 
demonstrated  by  the  following  experiments. 

If  lactic  acid  be  added  to  a  turbid  solution  of  lime- 
water,  the  lime  in  suspension  is  at  once  dissolved  and 
a  clear  solution  is  produced. 

The  same  occurs  when  phosphoric  acid  is  added  to  a 
turbid  solution  of  lime-water.  In  both  cases  the  lime 
is  converted  into  a  soluble  salt. 

5 


66  THE    GENESIS    OF    URIC    ACID 

Now  if  we  warm  lactic  acid  and  phosphoric  acid 
together,  there  is  no  violent  evolution  of  carbonic  acid 
gas,  but  if  we  add  a  drop  of  the  mixture  to  a  clear  solu- 
tion of  lime,  we  at  once  produce  a  precipitate,  showing 
that  carbonic  acid  gas  has  been  evolved  by  the 
combination.  Thus  we  know  that  if  by  any  means 
phosphoric  acid  is  set  free  from  the  phosphate  of  lime 
in  the  presence  of  lactic  acid,  carbonic  acid  is  produced. 
It  will  be  seen,  therefore,  that  the  purpose  served  by 
the  lime  in  the  laboratory  of  nature  is  to  set  free 
ammonia  from  its  combination,  and  that  of  the 
phosphoric  acid  to  oxidize  the  lactic  acid  and  convert 
into  carbonic  acid. 

As  a  further  test  for  my  conclusions,  I  tried 
to  produce  the  same  result  without  the  use  of  the 
phosphate  of  lime.  My  idea  was  that  we  should  be 
able  to  do  without  the  lime  if  we  supplied  an  acid 
carbonate  ready  made,  and  without  the  phosphoric 
acid  if  we  supplied  the  necessary  oxygen.  I  made 
some  lactate  of  ammonium  by  adding  ammonia  to  lactic 
acid,  and  when  chemical  reaction  had  ceased  I  intro- 
duced some  carbonate  of  ammonium,  which  caused 
great  effervescence.  When  this  had  subsided,  I  added 
peroxide  of  hydrogen  and  applied  heat.  There  was 
active  chemical  change,  and  when  it  had  ceased  I  made 
the  solution  acid  with  hydrochloric  acid.  After  leaving 
it  for  a  time,  I  put  a  drop  on  a  glass  slide  and  allowed 
it  to  evaporate.  When  dry  the  whole  field  was  covered 
with  crystals  of  lactate  of  ammonium.  I  redissolved 
these  crystals  in  peroxide  of  hydrogen,  and  in  a  short 
time  I  found  crystals  identical  in  form  with  uric  acid 
thrown  out  of  solution. 

I  allowed  the  preparation  to  dry,  and  after  twenty- 
four  hours  a  number  of  large  crystals  similar  in  shape 


THE    GENESIS    OF    URIC    ACID  67 

to  uric  acid,  with  decided  markings,  appeared.  From 
previous  experiments  I  recognized  these  crystals  as 
being  similar  in  composition  to  uric  acid,  but  containing 
excess  of  ammonia,  and  quite  soluble.  I  may  remark 
here  that  while  ammonia  in  excess  increases  the 
solubility  of  the  uric-acid  crystals,  it  renders  the  crystal 
of  lactophosphate  of  lime  less  soluble  ;  but  in  both 
cases  the  presence  of  ammonia  does  not  of  necessity 
alter  the  crystallization,  but  shows  itself  by  markings 


fig: 


on  the  face  of  the  crystals  as  if  they  had  been  roughly 
sculptured.  These  are  not  visible  in  the  minute  uric- 
acid  crystals  usually  met  with,  but  it  becomes  apparent 
when  larger  crystals  are  manufactured. 

To  the  dry  preparation  containing  these  large  soluble 
rhomboid  crystals,  I  added  strong  hydrochloric  acid. 
The  immediate  effect  was  the  deposition  of  small  uric- 
acid  crystals  in  large  quantities,  insoluble  in  strong 
hydrochloric  acid  (Fig.  28).  Now  it  is  evident  that  in 
this  experiment  I  had  too  much  ammonia  and  not 


68  THE    GENESIS    OF    URIC    ACID 

enough  acid  and  oxygen  in  my  original  solution,  but 
this  fact  makes  the  results  more  instructive,  as  it 
shows  more  clearly  the  factors  essential  to  the  genesis 
of  uric  acid. 

I  do  not  wish  it  to  be  inferred  from  these  experiments 
that  uric  acid  is  simply  a  lactocarbonate  of  ammonium, 
but  I  think  we  may  be  safe  in  saying  that  uric  acid  is 
formed  from  lactic  acid,  carbonic  acid,  and  ammonia 
by  the  action  of  oxygen  in  an  acid  solution,  and  that 
before  we  can  make  a  true  synthetic  product  we  require 
the  addition  of  the  colouring  matter  of  the  urine.  If 
I  were  a  chemist  I  might  express  myself  better  and  give 
chemical  formulae. 

I  think  the  true  importance  of  these  experiments  is 
to  bring  home  the  fact  that  while  attention  has  been 
drawn  to  the  insoluble  form  of  uric  acid,  on  account  of 
its  insolubility,  there  are  salts  containing  practically 
the  same  ingredients  which  are  soluble,  and  that  in 
the  human  subject  these  salts  are  formed  more 
frequently  than  the  insoluble  kind.  I  think  it  also 
shows  that  a  highly  acid  solution  is  necessary  to  the 
formation  of  the  insoluble  form. 

I  think  we  may  infer  from  these  experiments  that 
when  dealing  with  a  tendency  to  form  phosphate  of 
lime  calculi,  a  vegetable  dietary  which  may  increase 
the  excretion  of  ammonia  is  contra-indicated ;  and 
that  in  the  tendency  to  form  uric-acid  calculi,  the 
reverse  is  true.  In  fact,  I  have  used  chloride  of 
ammonium  with  great  advantage  in  cases  where  there 
was  a  tendency  to  excrete  uric  acid.  This  shows 
how  very  important  it  is  not  to  regard  chloride  of 
ammonium  as  the  agent  which  has  the  peculiar 
property  of  precipitating  urates,  as  is  stated  in  a 
recent  work  on  physiological  chemistry.  I  do  not 


THE    GENESIS    OF    URIC    ACID  69 

wish  the  reader  to  infer  that  I  regard  chloride  of 
ammonium  as  a  "  solvent  of  uric  acid  ".  There  is  no 
drug  or  chemical  which  can  dissolve  uric  acid  in  the 
body.  It  is  contrary  to  the  whole  scheme  of  nature, 
for  reasons  which  I  will  explain.  The  effect  of  the 
chloride  of  ammonium  is  to  prevent  the  formation  of 
the  insoluble  salt  of  uric  acid,  which  is  quite  another 
matter. 

Chemists  give  uric  acid  the  formula,  C5N4H4O3.  In 
Schafer's  Physiology  (p.  586)  it  is  stated  that, 
"  rightly  to  appreciate  the  physiology  no  less  than 
the  chemistry  of  uric  acid,  its  close  relationship  to 
urea  should  be  clearly  understood.  It  yields  the  latter 
by  a  combined  process  of  oxidation  and  hydrolysis  ". 
If  this  is  true,  the  urea  must  be  formed  from  the 
ammonium  carbonate  during  the  decomposition  which 
takes  place  when  uric  acid  is  formed.  Thus  it  is  only 
necessary  to  take  the  elements  of  water  from  ammo- 
nium carbonate  to  form  urea.  But  I  have  shown  that 
there  is  no  urea  in  the  so-called  ammonium  urate 
from  which  uric  acid  is  produced.  If  we  take  a  solu- 
tion of  prepared  urate  of  soda  and  add  to  it  a  few 
drops  of  Nessler's  solution,  we  shall  at  once  obtain 
an  orange-coloured  precipitate  indicating  the  presence 
of  ammonia.  Therefore  I  feel  justified  in  saying 
that  uric  acid  contains  no  urea. 

That  uric  acid  contains  lactic  acid  can  be  easily 
ascertained  by  boiling  a  little  uric  acid  with  some 
distilled  water,  and  then  adding  Uffelmann's  solution. 
The  blue  colour  is  instantly  discharged. 

We  have  now  to  consider  the  conditions  which  govern 
the  formation  of  uric  acid  as  a  product  of  the  human 
body.  All  the  ingredients  out  of  which  uric  acid  is 
made  exist  in  the  blood  ;  but  the  essential  conditions 


70  THE    GENESIS    OF    URIC    ACID 

under  which  they  can  undergo  the  necessary  combina- 
tion to  form  uric  acid  are  not  existent,  because  the 
fluids  of  the  body  are  alkaline  and  uric  acid  can  only 
be  produced  in  a  highly  acid  solution. 

But  it  is  also  part  of  the  scheme  of  nature  that  the 
fluids  of  the  body  and  the  products  of  katabolism 
shall  become  acid  immediately  before  excretion.  For 
this  purpose  the  kidneys  and  the  skin  are  provided 
with  the  necessary  apparatus  for  their  oxidation. 

It  appears  probable  that  this  is  a  necessary  pre- 
caution against  the  action  of  bacteria,  which  might 
easily  find  their  way  through  the  urinary  organs  to 
the  kidney  unless  means  were  taken  to  maintain  the 
excretion  in  a  state  of  acidity. 

Another  reason  is  that  while  the  excretory  organs 
render  the  fluids  which  pass  through  them  more  acid 
by  oxidation,  this  acidity  stimulates  the  excretory 
power  of  the  organ.  This  is  an  important  clinical 
fact.  It  can  be  illustrated  by  the  activity  of  the  skin 
excretion  in  a  case  of  rheumatic  fever. 

We  know  that  in  the  human  being  the  urea  passes 
through  the  kidney  unchanged,  in  spite  of  the  process 
of  oxidization  and  the  acid  medium  which  surrounds  it. 
I  have  demonstrated  that  it  is  able  to  do  this  because 
of  its  combination  with  sodium  chloride  ;  but,  just  as 
we  could  break  up  this  combination  in  the  laboratory 
by  the  use  of  strong  acids,  so  can  an  abnormal  condition 
of  the  urine  in  the  kidney  disassociate  the  sodium 
chloride,  set  free  the  urea,  and  produce  those  changes 
by  which  ammonia  is  formed,  which  I  have  already 
described. 

It  does  not  follow  that  these  chemical  combinations 
will  of  necessity  produce  uric  acid.  Normally,  in  the 
human  body,  it  does  not  do  so.  We  may  have  a  salt 


THE    GENESIS    OF    URIC    ACID  71 

formed  which  is  soluble  in  the  body  and  which  will 
remain  soluble  when  the  urine  is  cold.  Or  it  may  be 
soluble  at  the  temperature  of  the  body  and  be  thrown 
out  of  solution  as  the  urine  cools,  and  be  again  soluble 
when  heat  is  applied.  Or  we  may  have  a  salt  formed 
which  is  soluble  in  the  body,  but  which  is  precipitated 
as  the  urine  cools,  and  then  being  oxidized  by  the  air 
becomes  insoluble  when  heat  is  applied.  Or  we  may 
have — and  this  more  rarely  in  man — a  salt  formed  which 
is  insoluble  at  the  temperature  of  the  body  and  is 
excreted  as  a  solid.  This  is  normal  in  birds. 

It  is  the  less  soluble  combinations  which  have 
attracted  attention.  The  more  soluble  of  those  which 
we  call  lithates  or  urates,  are  regarded  as  of  little 
clinical  importance,  while  the  most  soluble  and  most 
normal  in  man  has  attracted  no  attention  at  all.  But 
this  highly  soluble  body  can  be  converted,  as  I  have 
shown,  into  the  insoluble  salt  by  the  addition  of  a 
mineral  acid  and  by  exposure  to  the  oxidizing  effects 
of  the  air. 

Here  we  have  the  fundamental  error  of  the  whole 
uric-icid  theory.  Because  the  chemist  can  manufacture 
uric  acid  from  normal  urine,  he  has  supposed  that  it 
already  existed  there.  This  conception  rendered  neces- 
sary the  existence  of  some  supposititious  base  with 
which  the  uric  acid  could  be  in  combination  and  so 
obtain  solubility.  In  this  way  the  urates,  biurates, 
and  quadriurates  came  to  exist  in  the  text-books,  but 
not  in  the  human  body.  In  the  course  of  these  investi- 
gations it  will  be  noticed  that  clinical  facts  difficult  to 
understand  become  perfectly  intelligible  and  natural 
directly  we  reach  the  physiological  truth.  We  can 
understand  now  why,  if  a  man  of  sedentary  habits 
takes  hard  physical  exercise  on  a  particular  day, 


72  THE    GENESIS    OF    URIC    ACID 

on  the  following  morning  his  urine  is  loaded  with 
lithates.  Some  part  of  this  may  be  due  to  the  great 
lymph-space  having  been  flushed  with  fluid,  causing  an 
increase  in  the  solid  matter  excreted.  But  this  does 
not  explain  all  the  facts.  This  matter  might  be  passed 
in  a  fluid  form,  and  we  should  only  notice  an  increase 
in  the  specific  gravity  of  the  urine.  But  we  may  have 
a  subnormal  specific  gravity  in  a  urine  which  deposits 
urates  directly  it  cools,  and  we  may  also  find  crystals 
of  uric  acid  in  the  deposit.  This  is  easily  intelligible 
when  we  remember  that  vigorous  exercise  causes  higher 
oxidation,  and  that  the  ingredients  which  enter  into 
the  composition  of  uric  acid  and  urates  are  consequently 
rendered  less  soluble.  This  also  explains  how  it  is  that 
foods,  which  contribute  nothing  to  the  ingredients  of 
which  uric  acid  is  composed,  have  been  proved  guilty 
of  increasing  the  quantity  of  uric  acid.  Red  meat, 
sugar,  and  alcohol  increase  the  oxidizing  power  of  the 
body,  and  therefore  result  in  an  augmentation  of  the 
salts  excreted  from  the  body  in  an  insoluble,  or  partially 
insoluble,  form. 

We  know  that  birds,  who  do  not  indulge  in  alcohol, 
sugar,  or  an  excess  of  red  meat,  have  a  urinary  excretion 
which  consists  of  little  else  but  uric  acid.  But,  owing 
to  the  large  amount  of  exercise  they  take  in  the  fresh 
air,  their  katabolic  products  must  be  very  highly 
oxidized,  and  they  must  also  form  a  large  amount  of 
lactic  acid.  The  urine  of  birds  is  passed  in  an  almost 
solid  form,  and  it  is  difficult  to  understand  how  this 
condition  is  compatible  with  its  passage  through  the 
kidney.  I  think  I  have  found  the  explanation  in  the 
following  experiment.  Uric  acid  is  very  soluble  when 
boiled  with  liquor  potassae.  If  a  strong  solution  of 
uric  acid  is  prepared  in  this  way  and  some  peroxide  of 


THE    GENESIS    OF    URIC    ACID  73 

hydrogen  is  added,  the  solution  is  converted  into  a 
semi-solid  mass.  This  occurs  instantaneously,  and  it 
is  easy  to  suppose  that  this  chemical  change  takes 
place  at  the  moment  of  excretion.  The  sudden  libera- 
tion of  phosphoric  acid  would  provide  the  necessary 
oxidizing  agent. 

We  may  now  ask  what  purpose  uric  acid  serves  in 
the  economy  of  nature.  I  know  that  we  are  taught  to 
regard  the  products  of  metabolism  not  only  as  waste 
matter  but  excrements  wholly  pernicious,  and  that  uric 
acid  is  regarded  as  the  worst  offender.  But  we  have 
seen  that  urea  has  useful  functions  to  perform  in 
maintaining  the  alkalinity  of  the  blood.  I  have  yet 
to  discover  any  evil  thing  it  accomplishes.  Lactic 
acid,  while  capable  of  causing  so  much  pain,  performs 
functions  which  we  have  seen  to  be  vitally  necessary. 
Both  these  are  soluble  bodies  capable  of  active  chemi- 
cal combinations.  Uric  acid,  on  the  other  hand,  is 
insoluble,  and  cannot  enter  into  combination  with 
the  salts  in  the  urine  or  with  the  tissues. 

This  is  the  rationale  of  its  existence.  This  will  be 
better  understood  if  we  consider  for  a  moment  the 
method  by  which  the  chemist  manufactures  uric  acid 
from  the  blood  or  the  urine.  He  simply  makes  it 
strongly  acid  and  leaves  it  exposed  to  the  air,  and 
then  all  the  chemical  processes  by  which  uric  acid  is 
made  go  on  automatically :  slower  under  these  con- 
ditions than  they  would  do  in  the  body,  but  still  they 
take  place. 

Now  suppose,  when  the  urine  has  been  rendered 
sufficiently  acid  to  produce  uric  acid,  instead  of  putting 
it  aside  in  a  warm  place  we  inject  it  back  into  the 
bladder,  the  result  would  be  a  very  violent  inflammation 
produced  by  an  excess  of  acid,  and  this  would  probably 


74  THE    GENESIS    OF    URIC    ACID 

prove  fatal.  But  such  a  state  of  intense  acidity  might 
easily  occur  in  the  kidneys,  because  it  is  part  of  their 
normal  function  to  increase  the  acidity  of  the  urine, 
and  there  are  many  conditions  which  cause  the  urine 
to  be  extremely  acid  when  it  reaches  them.  Nature 
has  to  provide  some  means  for  checking  this  process 
if  it  goes  too  far.  The  method  used  in  the  lymph  of 
making  the  increase  of  acid  produce  ammonia  would 
not  be  satisfactory,  because  it  is  necessary  that  the 
urine  should  retain  a  large  degree  of  acidity.  The 
method  adopted  is,  when  a  certain  stage  of  acidity  has 
been  reached,  to  lock  up  the  acids  in  an  insoluble  body 
which  can  be  excreted  without  exciting  any  inflam- 
matory effects  upon  the  mucous  membrane  of  the 
urinary  organs. 

It  is  for  this  reason  that  we  find  uric  acid  in  urine 
which  may  not  have  a  high  degree  of  acidity  because 
the  acids  are  locked  up.  In  such  urines,  if  the  acids 
were  liberated  from  the  uric  acid,  we  should  have  a 
highly  acid  solution. 

As  we  understand  the  nature  of  uric  acid,  we  see  the 
/  difficulties  created  by  the  false  conception  that  uric 
acid  exists  in  the  blood  ;  when  we  regard  it  as  a  safe- 
guard against  hyperacidity  of  the  urine,  we  can  com- 
prehend the  purpose  of  its  existence.  From  a  clinical 
standpoint  it  is  not  the  existence  of  uric  acid  in  the 
urine,  but  its  absence,  which  is  of  most  importance. 
When  uric  acid  appears  in  the  urine  we  know  that 
the  lactophosphates  are  being  excreted,  and  these  are 
necessary  to  the  manufacture  of  uric  acid.  It  is  the 
failure  of  this  excretion  which  causes  many  serious 
symptoms.  This  makes  the  chloride  and  hydroxide  of 
ammonium  test  one  of  the.  most  important  in  the 
examination  of  urine.  If  we  obtain  a  precipitate  with 


THE    GENESIS    OF    URIC    ACID  75 

these  reagents  we  need  not  trouble  ourselves  further, 
but  if  we  obtain  none  or  very  little  we  know  that  the 
kidney  is  failing  to  excrete  them.  This  failure  may 
cause  symptoms  which  are  obscure  until  the  cause  is 
known.  Thus,  attacks  of  giddiness  and  vertigo,  which 
occur  both  during  rest  and  during  exercise,  are  an 
indication  to  examine  the  urine,  and,  if  we  find 
diminished  excretion  of  phosphates,  we  may  be  fairly 
sure  it  is  the  cause  of  the  trouble.  The  same 
applies  to  some  forms  of  headache  and  drowsiness, 
and  also  high  blood-pressure.  If  the  patient  has 
lithates  in  the  joints,  the  effect  of  the  check  of 
excretion  will  be  to  set  up  chemical  changes  in  these 
lithates  and  cause  symptoms  of  '  gout '.  It  is  not 
uric  acid  which  produces  these  symptoms,  but 
the  soluble  lactophosphate  of  lime.  The  confusion 
between  these  two  bodies,  which  differ  so  widely  in 
their  physical  and  chemical  relations,  creates  a  diffi- 
culty in  understanding  the  clinical  symptoms  and 
the  effects  of  treatment.  The  true  position  is  this : 
uric  acid  begins  its  existence  in  the  kidney,  and 
then  only  under  uncommon  conditions,  and  termin- 
ates its  connection  with  the  body  when  the  urine  is 
excreted. 

Lactophosphate  of  lime  exists  in  every  fluid,  tissue, 
and  organ  of  the  body.  It  is  broken  up  in  the  process 
of  making  uric  acid,  but  this  can  only  be  accomplished 
in  a  very  acid  solution.  It  is  the  excretion  of  lacto- 
phosphate of  lime  which  is  of  importance,  and  it  is  a 
curious  fact  that  all  the  fluids  used  to  estimate  the 
excretion  of  uric  acid  contain  lactophosphate  of  lime 
and  no  uric  acid. 

It  will  be  observed  that  I  have  reached  conclusions 
respecting  the  physiology  and  chemistry  of  uric  acid 


76  THE    GENESIS    OF    URIC    ACID 

which  wholly  differ  from  the  statements  made  in  the 
extensive  literature  of  the  subject. 

It  would  occupy  too  much  space  to  enter  into  a  dis- 
cussion of  the  various  theories  put  forward.  They 
commence  with  the  assumption  that  uric  acid  can  be 
formed  in  the  alkaline  fluids  of  the  body,  and  then  go 
on  to  describe  uric  acid  as  performing  physical  and 
chemical  feats  of  which  an  insoluble  body  is  incapable. 
It  is  only  on  occasions  that  the  supposititious  soluble 
salt  of  uric  acid  is  introduced.  Thus,  it  is  not  until  we 
come  to  the  fourth  chapter  of  Haig's  work  on  uric 
acid  that  we  are  informed  that  "  uric  acid  in  the  title 
of  this  book,  and  generally  throughout  the  book  itself, 
unless  otherwise  specified,  is  used  as  an  inclusive  term 
comprehending  uric  acid  and  its  salts  ". 

This  makes  the  preceding  chapters  as  intelligible  as 
if  a  writer  on  therapeutics  insisted  upon  calling  Epsom 
salts  sulphuric  acid,  because  by  certain  chemical  ex- 
periments he  could  obtain  sulphuric  acid  from  these 
salts. 

But  even  with  this  explanation  we  are  still  left  in 
difficulties,  because  Haig  insists  that  the  urate  exists  in 
the  blood  in  an  insoluble  form.  He  says  : — 

"  Sir  Wm.  Roberts  says  (Urinary  and  Renal  Diseases, 
p.  73),  '  It  may  be  regarded  as  probable  that  the 
defective  power  of  the  kidneys  to  eliminate  uric  acid 
in  gout  arises  from  a  diminished  alkalescence  of  the 
blood '. 

"  From  my  point  of  view  it  has  nothing  whatever  to 
do  with  the  kidneys  ;  the  urates  are  not  in  solution  in 
the  blood,  and  are  not  brought  to  them  ;  when  they 
have  been  got  into  solution  by  an  alkali  they  are  ex- 
creted fast  enough." 

The  urate,  therefore,  is  considered  by  Haig  as  an 


THE    GENESIS    OF    URIC    ACID  77 

insoluble  body  which,  as  he  frequently  reiterates,  can 
be  rendered  soluble  by  a  single  dose  of  alkali,  and 
rendered  insoluble  (whatever  this  may  mean)  by  a 
single  dose  of  acid. 

But  Haig  admits  that  his  powers  to  produce  this 
marvel  have  limits.  On  page  15  he  tells  us  that 
"  though  I  could  produce  a  large  excretion  of  uric 
acid  at  pleasure  (by  the  administration  of  an  alkali),  I 
could  not  keep  up  the  excretion  very  long.  I  could 
produce  nothing  that  at  all  resembled  an  extra  forma- 
tion of  uric  acid  ". 

As  Haig's  conclusions  were  based  on  numerous  long 
and  laborious  experiments,  it  is  of  some  importance 
to  know  the  methods  by  which  he  reached  them. 
It  is  only  in  the  last  pages  of  the  book  that  these  are 
described.  He  estimated  the  quantity  of  uric  acid  by 
Haycraft's  method,  of  which  he  gives  a  complete 
description.  To  25  c.c.  of  urine,  15  gr.  of  bicarbonate 
of  soda  are  added  (Haig  used  30  gr.).  It  will  be  noticed 
that  this  differs  from  the  titration  test  in  the  fact  that 
in  the  latter  the  urine  is  saturated  with  chloride  of 
ammonium  to  ensure  its  alkalinity  ;  in  Haycraft's  test 
the  amount  of  alkali  added  had  no  reference  to  the 
degree  of  acidity  of  the  urine.  I  think  this  point  has  an 
important  bearing  upon  the  results  obtained  by  Haiff. 

The  sample  is  next  treated  with  2  to  3  c.c.  of  strong 
ammonia  and  about  2  c.c.  of  ammoniated  silver  nitrate 
solution.  This  brings  down  a  gelatinous  precipitate 
which  has  received  the  name  of  urate  of  silver.  Now 
nitrate  of  silver  has  no  more  power  to  precipitate  urea 
or  urates  than  ammonia  possesses,  but  both  have 
the  property  of  precipitating  lactophosphate  of  lime. 
Therefore  the  urate  of  silver  must  be  classed  with  the 
urate  of  ammonium  as  a  chemical  mistake.  The 


78  THE    GENESIS    OF    URIC    ACID 

solution  used  by  Haig  contained  no  urea,  nor  uric 
acid,  and  the  only  nitrogenous  product  was  the  am- 
monia he  added. 

The  precipitate,  after  being  filtered  and  washed  by  a 
tedious  process,  is  dissolved  in  nitric  acid  and  water, 
has  a  few  drops  of  ferric  alum  solution  added  to  act  as 
an  indicator,  and  the  ammonium  thiocyanate  solution  is 
added  until  a  permanent  pink  colour  is  produced. 

The  amount  of  '  uric  acid '  is  estimated  by  the 
amount  of  thiocyanate  solution  necessary  to  produce 
this  result.  In  both  chemical  methods  the  same 
mistake  has  been  made,  and  as  a  result  nitrogen,  a 
vital  necessity  of  nutrition,  has  been  made  to  appear  as 
a  source  of  evil,  and  has  been  charged  with  crimes  of 
which  it  is  wholly  guiltless. 


79 


CHAPTER    VI. 

EXCRETION. 

THE  great  lymph-space  which  lies  between  the  skin 
and  the  muscles  has  been  referred  to,  and  the  great 
importance  of  the  skin  as  an  organ  of  excretion  to 
eliminate  the  waste  products  which  are  formed  in  or 
discharged  into  this  space  will  be  appreciated. 

But  in  the  study  of  metabolism,  physiologists  have 
proceeded  on  the  assumption  that  all  the  waste  products 
of  proteid  metabolism  pass  through  the  kidney,  and 
that  as  a  result  we  can  estimate  the  amount  of 
nitrogenous  excretion  by  analysis  of  the  urine.  It  is 
well  known  that  urea  can,  and  does,  pass  through  the 
skin,  but  the  quantity  has  been  regarded  as  negligible. 
This  basic  hypothesis  is  distinctly  fallacious,  and  its 
fallacy  is  never  more  apparent  than  when  the  skin 
is  performing  its  functions  actively,  such  as  during 
vigorous  exercise. 

The  wide  difference  between  the  results  obtained 
and  the  actual  facts  is  well  known,  but  instead  of  this 
being  regarded  as  a  convincing  proof  that  the  method 
of  experiment  was  erroneous,  it  has  led  to  the  introduc- 
tion of  new  theories  to  explain  the  facts,  with  the  result 
that  an  altogether  unnecessary  confusion  has  been 
imported  into  the  whole  discussion. 

To  make  this  difficulty  understood,  I  will  quote  a  few 
paragraphs  from  Schafer's  Text-Book  of  Physiology, 
p.  912  :— 

"  The  most  interesting  question  in  connection  with  the 
special  metabolism  of  the  muscles  which  remains  to_be 


80  EXCRETION 

considered,  is  the  effect  which  their  exercise  produces 
upon  the  proteid  metabolism  of  the  body.  It  was  the 
opinion  of  Liebig  that  the  energy  of  muscular  contraction 
was  produced  by  the  oxidation  of  muscular  substance, 
and  it  would  follow  from  this  that  the  exercise  of  the  muscles 
must  tend,  ceteris  paribus,  to  increase  the  amount  of 
nitrogen  excreted  in  the  urine.  This  doctrine  of  Liebig's 
was  accepted  for  many  years  by  physiologists,  but  was, 
for  a  time  at  least,  completely  overthrown  by  the  results 
of  the  famous  experiment  of  Fick  and  Wislicenus,  known 
as  the  experiment  of  the  ascent  of  the  Faulhorn.  It  was 
shown  by  these  observers  that  at  least  three  times  as  much 
work  was  done  during  the  ascent  as  could  be  accounted 
for  by  the  oxidation  of  proteid,  as  estimated  by  the  amount 
of  nitrogen  eliminated  by  them  during  and  after  the  work. 
"  The  work,  therefore,  could  only  have  been  caused  by 
the  oxidation  of  non-proteid  matter.  Similar  results 
were  obtained  by  Parkes  and  others  in  man,  and  by 
C.  Voit  in  dogs.  This,  combined  with  the  fact  that  the 
CO.,  output  of  the  body  is  increased  in  proportion  to  the 
amount  of  exercise,  led  to  the  view  being  widely  adopted 
that  the  energy  of  the  body  is  mainly,  if  not  entirely, 
obtained  by  oxidation  of  non-proteid  materials,  and  that 
the  splitting  and  oxidation  of  proteid  must  contribute, 
under  the  ordinary  circumstances  of  a  mixed  diet,  but 
little  to  the  production  of  muscular  energy." 

Extract  from  the  same  book,  p.  904  : — 

"  That  the  change  in  proteid  which  results  in  the 
formation  of  urea  must  primarily  occur  within  the  muscles, 
within  which,  as  we  have  seen,  the  greater  part  of  the 
oxidations  of  the  body  occur,  there  can  be  very  little 
doubt.  But  there  has  always  been  this  difficulty  in 
connection  with  the  question,  that  although  urea  is  the 
ultimate  product  of  proteid  metabolism,  the  muscles 
practically  contain  either  no  urea,  or  only  a  very  small 
amount." 

With  reference  to  these  difficulties,  I  can  speak 
from  personal  experience  of  the  physiological  effects 
of  climbing  mountains.  For  many  years,  after  a 
sedentary  life  during  eleven  months  of  the  year,  I  went 
during  the  month  of  August  to  Switzerland,  or  some 
other  mountainous  country,  and  walked  as  straight  as 
possible  across  the  country,  taking  the  mountains  as  -I 


EXCRETION  81 

came  to  them.  The  most  important  physiological 
effect  observed  was  naturally  that  of  the  excretions  of 
the  skin :  the  sweat  from  the  face  alone  would  leave  a 
track  as  I  walked.  It  will  be  observed  that  the  ex- 
cretion of  the  skin  is  not  mentioned  in  the  '  famous 
experiment '  cited  above,  which  is  recorded  in  most 
of  the  physiological  text-books. 

Another  important  fact  was  that  the  temperature  of 
the  body  was  raised  from  i°  to  2°  F.,  showing  that 
very  active  chemical  changes  were  taking  place  in 
the  tissues.  This  fact  is  also  left  out  of  account. 

The  greater  elimination  of  carbonic  acid  gas  which 
naturally  resulted  from  these  ascents  is  mentioned,  but 
the  important  fact  that  the  urine  was  much  diminished 
in  amount,  owing  to  the  excessive  sweating,  was  not 
noticed.  After  the  first  day  there  was  no  appearance 
of  urates,  nor  any  increase  of  colour  to  indicate  that  the 
urine  was  more  concentrated.  I  did  not  examine  the 
urine  for  nitrogen.  The  idea  that  the  amount  it  con- 
tained was  an  index  of  the  work  accomplished  appeared 
to  me  a  preposterous  proposition. 

It  is  perfectly  obvious  that  my  muscles  were  throwing 
out  a  large  quantity  of  lactic  acid,  and  this  would 
convert  the  urea  into  ammonia,  and  this  ammonia 
would  find  its  outlet  by  the  skin  and  the  lungs. 

The  enormous  amount  of  nitrogen  which  is  lost 
through  the  skin  and  the  lungs  in  the  form  of  ammonia 
has  never  been  taken  into  account  in  any  of  these 
experiments.  Yet  this  ammonia  is  very  evident  to 
the  senses  if  we  enter  a  barrack-room  when  soldiers 
have  just  come  back  from  a  march.  Parkes,  in  his 
work  on  Practical  Hygiene  (p.  104),  mentions  this,  and 
also  notes  that  there  was  no  augmentation  in  carbonic 
acid  gas.  Parkes  also  quotes  some  experiments  made 


82  EXCRETION 

by  Moss  on  the  air  of  a  military  hospital.  He  found 
that  the  quantity  of  ammonia  in  milligrammes  per  cubic 
metre  was  0-855,  an(i  °f  albuminoid  ammonia  1-307. 

But  the  excretion  of  ammonia  must  not  be  regarded 
as  only  occurring  after  exercise.  I  find  it  very  fre- 
quently present  in  the  sweat  of  patients  confined  to 
bed,  and  it  can  at  any  moment  and  under  all  conditions 
be  found  in  the  air  expired  from  the  lung.  It  is 
only  necessary  to  place  a  drop  of  hydrochloric  acid  on 
a  glass  slide,  allow  it  to  become  nearly  dry,  and  then 
breathe  upon  it  (see  Plate  VI,  Fig.  29).  We  shall 
at  once  obtain  crystals  of  chloride  of  ammonium. 
Ammonia  is  exhaled  in  a  free  state  from  the  skin. 
This  can  be  demonstrated  by  taking  some  cotton 
material  and  soaking  it  in  phenol-red ;  as  it  dries  in 
the  air,  it  will  be  turned  yellow  by  the  carbonic  acid 
gas  present.  If  this  is  placed  at  the  bottom  of  a  pill- 
box and  the  box  attached  to  the  skin  so  that  the 
yellow  cotton  does  not  come  in  contact  with  the 
skin,  the  ammonia  evolved  will  react  on  the  colour 
of  the  cotton  and  turn  it  red.  This  effect  is  best 
observed  during  exercise,  or  when  the  patient  is  in  a 
vapour  bath. 

But  now  we  come  to  another  riddle  of  physiology, 
which  has  led  to  the  introduction  of  theories  that 
have  been  the  cause  of  much  controversy.  As  urea  is 
the  ultimate  product  of  the  katabolism  of  protoplasm, 
why  do  we  not  find  it  in  the  muscles  ?  If  we  adopt  the 
theory  that  the  energy  of  the  muscles  is  due  to  non- 
proteid  material,  i.e.,  the  carbohydrates,  we  have  still 
to  account  for  the  dead  cells  of  the  muscles,  which  must 
contain  proteid  matter.  There  is  no  doubt  that  urea 
is  not  only  formed  in  the  muscles  but  must  occur  in 
large  quantities. 


PL  A  TE     VI. 


• 


fig.  29. 


EXCRETION  83 

The  fact  that  the  chemist  fails  to  find  it  is  no  proof 
to  the  contrary.  That  the  urea  formed  must  come  in 
contact  with  lactic  acid  is  certain,  and  if  so  it  would 
be  converted  into  ammonia ;  but  if  this  were  the  regular 
course  we  should  produce  a  great  deal  more  ammonia 
than  we  do,  and  man  would  become  a  very  unsavoury 
animal. 

The  normal  product  of  muscular  contraction  is  car- 
bonic acid  gas.  What  effect  would  this  have  upon  the 
urea  ? 

Finding  no  information  on  the  point,  I  made  a  solu- 
tion of  urea  and  passed  a  stream  of  carbonic  acid  gas 
through  it.  I  then  examined  the  solution  under  the 
microscope.  I  did  not  find  urea;  I  did  not  find  any 
combination  of  urea ;  I  found  nothing.  Obviously 
the  carbonic  acid  gas  had  broken  up  the  urea  into  its 
ultimate  elements — carbonic  acid  gas  and  nitrogen. 

To  look  for  urea  in  muscle  is  like  seeking  the  paper 
with  which  the  servant  lighted  the  fire  in  the  morning  ; 
and  failing  to  find  it,  evolving  a  theory  that  she  had 
discovered  a  way  of  lighting  the  fire  without  paper. 
What  becomes  of  the  nitrogen  produced  ?  The  bulk 
of  it  unquestionably  is  got  rid  of  by  the  skin,  although 
some  may  find  its  way  through  the  lungs. 

It  will  be  seen  therefore  that  experiments  to  deter- 
mine the  amount  of  nitrogen  eliminated  which  depend 
upon  the  quantity  existing  in  the  urine  are  entirely 
fallacious  ;  practically  the  whole  of  the  nitrogen 
evolved  from  muscular  contraction  is  not  taken  into 
account. 

But  if  we  could  measure  all  the  free  nitrogen,  ammonia, 
and  urea  eliminated  by^the  skin  and  the  lungs  during 
severe  exercise,  and^add  it  to  that  obtained  from  the 
urine,  I  think  the  amount  would  not  equal  the  energy 


84  EXCRETION 

expended.  I  think  so,  because  during  my  walks,  which 
lasted  from  seven  to  ten  days,  the  amount  of  food  taken 
was  not  equivalent  to  the  energy  expended.  There 
was  always  a  marked  absence  of  desire  for  food.  A  roll 
and  butter  at  6  a.m.  and  the  usual  continental  sandwich 
during  the  day  was  all  I  found  necessary.  The  usual 
supper  was  soup,  omelette,  and  cheese.  It  was  not  a 
loss  of  appetite  from  over-fatigue,  but  rather  from  the 
sense  of  being  fully  satisfied,  as  one  might  feel  soon 
after  a  good  meal. 

I  have  met  with  many  others  who  on  their  mountain 
excursions  had  the  same  feelings,  which  they  ascribed 
to  '  living  on  the  air  '.  But  this  explanation  is  not 
correct,  because  visitors  at  the  high  mountain  resorts 
who  spend  most  of  their  time  out  of  doors  do  ample 
justice  to  the  excellent  fare  provided,  as  I  do  myself 
during  the  periods  of  rest. 

There  can  be  no  doubt  that  during  great  and 
prolonged  physical  exertion,  also  during  fever,  some 
products  of  metabolism,  normally  excreted,  are  used 
as  a  source  of  energy.  This  is  altogether  apart  from 
nourishment  derived  from  destructive  changes  in  the 
tissue,  as  during  starvation.  It  seems  possible  that  the 
nitrogen  set  free  in  the  muscles  by  the  destruction  of 
the  urea  is  partially  reabsorbed  and  utilized  to  supply 
the  demand  for  nitrogen  which  exists  under  these 
circumstances.  In  no  other  way  can  I  understand 
how  a  man  in  perfect  health,  and  creating  that  demand 
by  vigorous  exercise,  is  satisfied  without  taking  the 
extra  amount  of  food  regarded  as  theoretically  neces- 
sary, and  desires  considerably  less  than  would  be  taken 
by  a  person  of  sedentary  habits. 

Physiologists  have  never  sufficiently  recognized  the 
skin  as  an  organ  of  excretion.  The  sweat  ducts  have 


EXCRETION  85 

been  described  as  having  a  '  secretion '  of  their  own, 
chiefly  consisting  of  salt  and  water,  but  it  is  recognized 
that  urea  and  other  products  have  been  found  in  the 
sweat.  The  sebaceous  glands  have  been  described  as 
secreting  various  fatty  acids.  The  capillaries,  by  their 
dilatation,  are  known  to  liberate  heat  from  the  body 
and  by  their  contraction  to  retain  it,  but  they  are 
not  recognized  as  part  of  the  machinery  for  oxidizing 
the  waste  products  in  the  great  lymph-space  beneath 
them. 

Functional  inactivity  of  the  oxidizing  and  excretory 
powers  of  the  skin  is  the  cause  of  many  ailments  the 
physician  is  called  upon  to  treat — and  fails  to  relieve 
because  the  cause  is  not  recognized.  If  we  watch  the 
life  history  of  those  who  suffer  from  this  physiological 
deficiency,  we  shall  find  that  eventually  some  form 
of  nephritis  gives  expression  to  the  condition,  and 
the  life  of  the  patient  is  shortened.  We  try  by  diet  to 
prevent  the  accumulation  of  '  uric  acid '  in  the  tissues, 
but  take  no  steps  to  provide  for  its  elimination  by  the 
skin. 

Long  clinical  experience  has  led  me  to  connect 
the  persistent  subnormal  temperature  with  imperfect 
performance  of  the  functions  of  the  skin.  There  are 
doubtless  other  causes  of  a  subnormal  temperature; 
but  when  we  find  a  patient  in  good  health,  and  all 
the  other  functions  performed  properly,  with  a  persistent 
subnormal  temperature,  we  may  suspect  that  the 
functions  of  the  skin  are  in  abeyance. 

When  the  skin  is  excited  to  a  large  degree  of  activity, 
as  during  vigorous  exercise,  the  temperature  of  the 
body  rises  above  normal.  I  do  not  claim  that  the  whole 
of  the  rise  of  temperature  is  produced  by  the  oxidizing 
processes  taking  place  in  the  skin,  but  it  is  obvious 


86  EXCRETION 

that  these  processes  could  not  be  going  on  over  the 
whole  surface  of  the  body  without  causing  a  rise 
of  temperature.  Therefore  we  must  not  regard  the 
skin  as  a  simple  regulator  of  heat,  but  as  a  source  of 
heat,  and  this  point  is  of  great  clinical  importance, 
because  if  we  keep  the  skin  warm  we  increase  its 
functional  activity,  and  this  activity  becomes  a  source 
of  heat. 

Before  considering  the  matters  excreted  by  the  skin, 
it  is  important  to  remember  that  the  act  of  sweating 
is  of  two  distinct  kinds.  Visible  fluid  may  be  made  to 
appear  on  the  skin  as  a  result  of  purely  nervous  influence, 
such  as  pain,  emotion,  or  shock.  We  may  produce 
copious  sweating  by  the  application  of  very  high 
temperature  to  the  nerves  of  the  skin,  such  as  would 
be  produced  in  the  hottest  room  of  the  Turkish  bath. 
Sweating  produced  by  such  causes  is  not  accompanied 
by  any  rise  in  the  body  temperature,  the  fluid  excreted 
is  chiefly  salt  and  water,  and  although  it  may  carry 
with  it  any  matter  which  may  exist  in  the  ducts  them- 
selves, or  in  the  lymph-space  beneath,  it  does  not  set 
free  the  lactic  acid  which  is  locked  up  in  the  tissues 
of  the  body  or  in  a  state  of  combination.  The  other 
form  of  sweating  represents  a  real  increase  in  functional 
activity,  rather  than  a  paresis  ;  it  occurs  after  vigorous 
exercise,  as  the  effect  of  moderate  degrees  of  heat,  and 
when  radiation  is  checked  either  by  clothing  or  moisture 
in  the  air.  This  sweating  is  always  accompanied  by  a 
rise  of  temperature  of  the  body,  and  represents  its 
normal  function. 

Both  by  physiologists  and  clinically  these  two  forms 
of  sweat  production  have  been  confused.  They  are 
physiologically  distinct,  and  the  resulting  excretion 
has  not  the  same  chemical  composition. 


87 


Schafer  (Text-Book  of  Physiology,  p.  671)  gives  the 
chemical  analyses  of  what  he  calls  the  '  secretion  of  the 
skin ',  made  by  three  different  chemists. 


In   1000  parts. 

FAVRE. 

SCHOTTIN. 

FtJNKE. 

Water 

995*573 

977-40 

988-40 

Solids 

4-427 

22'6O 

II-60 

Epithelium 

— 

• 



Fat  .. 

•013 

• 



Lactatcs     . 

'Si? 

• 



Sudorates  . 

1-562 





Extractives 

•005 

II-30 



Urea 

•440 

— 

I'55 

Sodium  chloride 

2-230 

3-60 



Potassium  chloride 

•240 



— 

Sodium  phosphate 

•Traces 

I-3I 



Alkaline  sulphates 

•no 

•39 



Earthy  phosphates 

Traces 

— 



Total  salts 

7-00 

4'36 

It  will  be  observed  that  there  is  a  wide  difference 
between  the  results  obtained  by  different  observers. 
This  is  inevitable,  because  there  is  no  constancy  in  the 
composition  of  the  sweat.  It  is  seldom  precisely  the 
same  in  any  two  individuals  ;  it  may  vary  in  the  same 
individual  at  different  periods  of  the  day,  according 
to  physical  conditions,  and  it  may  also  vary  in  different 
parts  of  the  body  in  the  same  individual  at  the  same 
moment. 

Chloride  of  sodium  is  always  stated  to  be  the  chief 
component  of  the  sweat.  This  is  only  true  in  chemical 
language.  Crystals  of  pure  chloride  of  sodium  are  met 
with  very  infrequently  in  the  sweat.  They  usually 
occur  at  the  end  of  very  profuse  sweating  or  in  the 
sweat  of  paresis  or  of  very  high  temperature. 

Chloride  of  sodium   is    almost   invariably   found   in 


88  EXCRETION 

combination  with  other  bodies.  We  have  already  dis- 
cussed its  combination  with  urea,  and  the  crystals 
described  are  observed  with  great  frequency  in  the 
sweat,  and  enable  us  to  judge  the  amount  of  urea 
present.  It  is  well  to  remember  that  the  presence  of 
the  urea-sodium-chloride  dagger  crystals  does  not  imply 
a  very  small  proportion  of  urea  if  the  minute  urates  are 
also  present,  as  they  usually  are. 

In  the  chapter  on  lactic  acid  I  have  described  and 
illustrated  the  combination  of  sodium  chloride  with 
lactic  acid.  The  form  most  frequently  met  with  in 
the  sweat  is  the  one  like  a  scaling-ladder  with  a 
number  of .  lateral  rods  of  unequal  length.  It  has 
some  resemblance  to  the  lactochloride  of  ammonium. 
When  any  doubt  occurs,  it  may  be  cleared  up  by 
adding  a  drop  of  Nessler's  solution  to  the  specimen, 
when,  if  the  ammonia  salt  is  present,  an  orange- 
coloured  precipitate  will  be  formed.  I  have  never 
found  chloride  of  ammonium  except  in  combination 
with  lactic  acid. 

The  photograph  of  a  drop  of  sweat  (Plate  VII, 
Fig-  3°)  shows  urea  in  combination  with  chloride  of 
sodium  in  the  proportion  of  one  to  eight.  At  the 
lower  part  of  the  plate  we  see  excellent  crystals  of 
lactochloride  of  ammonium.  This  also  demonstrates 
that  the  urate  was  able  to  be  formed  because  the 
lactic  acid  was  locked  up  by  the  chloride  of  am- 
monium. 

Only  one  of  the  chemists  whose  analyses  we  have 
quoted  has  apparently  found  lactic  acid  in  the  sweat, 
but  it  appears  in  so  many  forms  that  its  entire 
absence  is  very  rare.  In  addition  to  existing  in  combin- 
ation with  chloride  of  sodium  and  ammonium,  it  also 
appears  as  the  lactophosphate  of  lime.  This  salt  in  its 


PLATE     VII. 


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*  ,       *         '    »     »  *•«-••' 

•*  *'.•  .».!.f -.?;'*•  «     »-•* 

•  %.      ****'"  **.*•*  .**  V  * 

' ?  »  *  *J>      »•*«****      -.  * 

>£%£<  BV7.^.-A.*'     . 

-:.-;  i.v ;.-••;  .v-^.1 

..  '/:':.*\'**  ;\*i>:* 


Fie.    31- 


EXCRETION  89 

unoxidized  form  is  usually  found  in  large  quantities 
in  the  sweat  of  rheumatic  patients,  although  its  exis- 
tence appears  to  have  passed  unnoticed. 

Fig.  31,  Plate  VII,  is  a  negative  of  the  sweat  of  a 
rheumatic  patient,  wholly  consisting  of  minute  urates, 
which  do  not  appear  in  the  photograph,  and  soluble 
lactophosphate  of  lime. 

But  there  is  still  another  combination  of  lactic  acid 
found  in  the  sweat,  which  also  may  exist  in  large  quanti- 
ties. This  is  the  acid  lactate  of  ammonium.  I  have 
already  explained  that  when  free  lactic  acid  enters  the 
lymph-space  in  large  quantities  it  may  combine  with 
urea,  because  the  urate  cannot  be  formed  in  an  acid 
solution.  It  converts  it  into  lactate  of  urea,  which 
passes  rapidly  into  lactate  of  ammonium.  I  have  never 
found  a  crystal  of  lactate  of  urea  either  in  the  sweat 
or  the  urine. 

Lactate  of  ammonium  has  an  alkaline  reaction,  and 
turns  litmus  paper  blue  in  spite  of  the  large  quantity 
of  lactic  acid  it  contains,  owing  to  the  remarkable 
power  which  ammonia  possesses  of  neutralizing  lactic 
acid.  Therefore  an  alkaline  reaction  to  litmus  paper 
is  no  proof  of  the  non-existence  of  lactic  acid.  The 
difficulty  this  would  otherwise  present  is  diminished 
by  the  fact  that  it  is  nearly  always  present  as  an  acid 
lactate  of  ammonium,  and  this,  instead  of  turning  litmus 
paper  red,  gives  it  a  salmon-pink  appearance,  which  is 
diagnostic  of  the  presence  of  acid  lactate  of  ammonium. 
But  we  meet  with  conditions  when  the  sweat  turns 
litmus  paper  neither  red  nor  blue,  but  decolorizes  it  and 
leaves  an  almost  white  surface.  This  is  due  to  a  more 
highly  oxidized  form  of  lactate  of  ammonium,  and 
represents  a  very  large  amount  of  lactic  acid  in  the 
tissues  and  the  lymph-space.  These  facts  caused  me 


90  EXCRETION 

some  trouble  before  I  understood  them,  and  their  im- 
portance for  diagnostic  purposes  is  very  great. 

I  have  already  alluded  to  the  very  large  amount  of 
ammonia  which  is  excreted  by  the  skin  under  certain 
conditions.  It  occurs  in  the  sweat  with  such  great 
frequency  that  it  is  remarkable  that  none  of  the  analyses 
of  the  sweat  contain  any  mention  of  it. 

It  is  only  by  constant  observation  of  a  large  number 
of  specimens  of  sweat  and  under  different  conditions 
that  we  can  really  gain  any  information  about  it,  and 
then  we  shall  be  impressed  with  the  very  wide  varia- 
tions which  exist  in  its  chemical  constituents. 

It  would  be  impossible  to  make  a  quantitative 
analysis,  and,  if  we  did,  the  facts  elicited  are  not  very 
helpful;  but  the  method  I  have  described  enables  a 
dozen  specimens  of  sweat  to  be  examined  and  reported 
upon  in  the  course  of  an  hour,  and  the  knowledge 
obtained  is  exact. 

When  we  have  done  so,  no  doubt  can  be  left  in  our 
minds  that  we  are  dealing,  not  with  the  secretion  of  a 
gland  or  a  duct,  but  with  the  constituents  of  the  great 
lymph-space  which  lies  beneath  the  skin ;  and  we  can 
go  further  than  that,  and  say  we  are  observing  the 
actual  products  formed  in  the  tissues  immediately 
beneath  the  point  whence  the  sweat  was  taken.  It 
may  be  a  little  difficult  to  believe  this  at  first,  but  the 
following  observations  give  it  proof. 

The  reaction  of  the  sweat  has  been  described  as 
both  alkaline  (Sir  Michael  Foster)  and  acid  (Schafer). 
Both  observers  may  be  right,  because  the  reaction  varies 
with  the  part  of  the  skin  whence  the  reaction  is  taken. 
The  skin  is  sometimes  neutral,  rarely  decidedly  alka- 
line, more  generally  very  slightly  acid  if  taken  over 
the  chest  wall.  In  the  same  person,  at  the  same  time, 


EXCRETION  91 

the  reaction  of  the  skin  of  the  palm  of  the  hand  may 
show  some  acidity,  while  the  sole  of  the  foot  may  be 
decidedly  acid. 

Except  when  there  is  some  marked  and  general 
production  of  lactic  acid,  we  never  find  the  same  degree 
of  acidity  over  the  whole  skin.  As  a  general  rule  the 
extremities,  hands  and  feet,  are  more  acid  than  the 
remainder  of  the  body,  and  the  feet  more  acid  than 
the  hands ;  but  the  forehead  has  usually  a  smaller 
degree  of  acidity  than  either. 

Although  there  are  differences  in  the  reaction  of  the 
skin  in  different  parts  of  the  body,  the  records  taken 
of  patients  who  are  under  treatment  present  a  certain 
uniformity. 

The  rheumatic  patient  has  a  very  acid  reaction  at 
the  outset,  and  this  may  continue  for  an  indefinite 
time,  according  to  the  nature  of  the  case.  Then  there 
comes  a  steady  diminution  in  the  degree  of  acidity, 
until  the  reaction  becomes  very  slightly  acid  or  neutral. 

The  patient  with  the  lithic  diathesis  runs  an  entirely 
different  course.  His  reactions  are  neutral  or  very 
slightly  acid  at  the  outset,  and  gradually  increase  in 
acidity  until  they  reach  a  certain  point,  when  they 
begin  gradually  to  diminish  in  acidity  until  they  are 
neutral  or  very  slightly  acid. 

If  we  take  fifty  charts  on  which  the  skin  reactions  are 
recorded,  it  is  quite  easy  to  sort  out  those  of  rheu- 
matic from  those  of  gouty  patients,  without  knowing 
anything  about  the  patients  or  their  symptoms.  I 
know  of  no  way  which  enables  us  so  clearly  to  dis- 
tinguish between  the  two  classes  of  cases. 

The  fact  that  a  patient  with  gout  has  had  a  very  acid 
reaction  and  it  has  come  down  to  neutral  is  no  indica- 
tion that  the  lithates  have  been  completely  removed ; 


92  EXCRETION 

it  only  means  that  we  have  got  rid  of  all  his  additive 
lactic  acid,  and  in  the  course  of  doing  so  have  removed 
as  much  of  the  lithates  as  the  acid  set  free  was  capable 
of  doing. 

It  is  better,  therefore,  to  discontinue  treatment  and 
wait  some  months  before  renewing  it,  and  this  may  be 
rendered  unnecessary  by  the  improvement  that  has 
taken  place  in  the  functions  of  the  skin.  In  many 
cases  the  lithates  subsequently  disappear  without 
further  treatment. 

I  began  making  experiments  on  these  points  some 
twenty-five  years  ago,  and  I  found  them  so  helpful, 
both  for  purposes  of  diagnosis  and  as  a  guide  to 
treatment,  that  I  have  continued  them  as  a  matter 
of  routine  ever  since.  As  over  a  hundred  such  observa- 
tions are  made  and  recorded  every  day,  I  can  speak 
on  this  subject  with  some  authority.  I  could  give 
many  instances  to  show  that  the  chemical  composition 
of  the  sweat  immediately  over  any  part  of  the  body  is 
influenced  by  the  processes  taking  place  in  the  tissues 
beneath  it ;  but  one  which  any  practitioner  can  observe 
for  himself  is,  I  think,  conclusive. 

If  a  piece  of  litmus  paper  is  moistened  and  applied 
to  a  joint  during  an  attack  of  acute  gout,  it  will 
give  an  intensely  acid  reaction.  If,  now,  the  same 
experiment  is  made  at  a  point  on  the  skin  a  few 
inches  away  from  the  joint,  the  reaction  may  be 
only  slightly  acid.  Personally  I  use  for  experimental 
purposes  discs  of  cotton  material  which  has  been  soaked 
in  phenol-red  and  dried.  In  the  process  they  turn 
yellow,  and  in  this  state  are  valuable  for  testing  for 
ammonia,  but  for  determining  the  acid  reaction  of  the 
skin  they  are  kept  in  a  bottle  containing  ammonia, 
which  restores  the  pink  colour. 


EXCRETION  93 

When  moistened  and  placed  on  the  skin,  the  time 
taken  for  the  disc  to  turn  yellow  affords  a  very  good 
indication  of  the  degree  of  acidity. 

I  have  occupied  much  of  the  reader's  time  in  discuss- 
ing various  chemical  and  physiological  problems,  but  I 
have  tried  to  keep  to  the  facts  which  have  a  direct 
clinical  bearing  upon  the  study  and  treatment  of  the 
rheumatic  and  gouty  disorders.  With  the  knowledge 
gained  from  these  simple  experiments  we  can  approach 
the  subject  with  a  better  understanding  of  the  problems 
with  which  we  have  to  deal,  and  work  out  the  right 
line  of  treatment  which  the  conditions  present  in  the 
individual  patient  suggest. 


94 


CHAPTER    VII. 

RHEUMATISM   AND   THE    LACTIC-ACID 
DIATHESIS. 

THE  term  rheumatism  is  applied  to  a  painful  condition 
of  the  joints  or  tissues  which  may  exist  with  or  with- 
out a  rise  of  temperature.  It  is  one  of  the  symptoms 
of  an  underlying  condition,  but  not  a  necessary  one, 
for  the  state  of  the  tissues  which  causes  rheumatism 
may  produce  other  symptoms,  or  no  symptoms  at  all. 

We  associate  rheumatism  in  its  acute  form  with  an 
exceedingly  acid  condition  of  the  cutaneous  excretion, 
and  we  know  that  the  cause  of  this  acidity  is  an  excess 
of  lactic  acid.  But  an  intense  acidity  of  the  skin  is 
compatible  with  an  appearance  of  perfect  health  ;  in 
fact  we  commonly  find  these  symptoms  in  persons  who 
appear  to  be  exceptionally  robust.  If,  however,  we 
watch  the  life-history  of  such  people,  we  shall  have  a 
much  clearer  understanding  of  the  nature  of  the  disorder, 
and  shall  observe  that  these  persons  are  more  liable 
than  others  to  suffer  from  certain  ailments. 

An  excessive  acidity  of  the  skin  proves  not  only  that 
the  person  is  producing  an  excessive  amount  of  lactic 
acid,  but  also  that  he  is  able  to  excrete  it.  This  capacity 
for  excretion  may,  under  some  conditions,  cause  trouble. 
We  may  find  that  the  skin  becomes  raw  and  abraded 
from  the  action  of  the  acid  lying  in  contact  with  it,  and 
this  occurs  most  frequently  where  two  portions  of  the 
skin  are  normally  in  close  apposition.  We  call  this 
eczema,  and  if  we  apply  the  usual  ointments  may  find 


RHEUMATISM    AXD    LACTIC    ACID          95 

it  difficult  to  cure  because  we  have  not  removed  the 
cause  of  the  condition.  If  we  employ  a  calamine  lotion 
or  some  alkaline  powder  or  adopt  any  means  by  which 
the  excretion  is  prevented  from  irritating  the  skin,  we 
can  relieve  the  local  symptom  although  we  have  not 
removed  the  cause,  but  the  success  of  such  treatment 
will  make  the  cause  clear  to  us. 

It  must  not  be  inferred  from  this  that  I  tiace  all 
cases  of  eczema  to  an  excessive  acidity  of  the  skin.  On 
the  contrary,  some  of  the  most  inveterate  cases  I  have 
seen  are  those  in  which  the  excretory  powers  of  the 
skin  are  almost  completely  in  abeyance.  When,  in 
such  cases,  we  cause  the  functions  of  the  skin  to  be 
resumed,  we  at  first  find  neither  urea  nor  lactic  acid 
excreted,  but  I  have  found  formic  acid,  which  will 
account  for  the  intense  irritation  of  the  skin  generally 
observed  in  these  cases.  The  sweat,  when  the  excretion 
is  first  resumed,  has  the  appearance  of  milk,  owing  to 
the  enormous  number  of  epithelial  scales  which  are 
present. 

This  is  a  digression  from  rny  subject,  but  it  may  serve 
to  call  attention  to  the  fact  that  the  treatment  of  skin 
diseases  without  any  attempt  to  study  the  condition 
of  the  cutaneous  excretions  and  to  remedy  any  defect 
which  may  exist  in  the  performance  of  the  functions  of 
the  skin  must  lead  to  failure. 

Excessive  acidity  of  the  skin  is  found  under  two 
different  conditions.  There  is  an  acid  sweat  which  only 
appears  as  a  result  of  active  exercise  or  from  the  effect 
of  the  temperature  to  which  the  body  is  exposed,  and 
there  is  also  a  passive  excretion  of  acid  sweat  which 
may  continue  without  the  presence  of  any  agency  to 
excite  it. 

The  first  is  due  to  the  physiological  activity  of  all  the 


96  RHEUMATISM    AND    THE 

factors  concerned  in  the  skin  excretion,  and  removes  the 
additive  lactic  acid  from  the  tissues.  The  second  is  due 
to  an  excess  of  free  lactic  acid,  stimulating  the  excretory 
functions  of  the  skin,  but  depressing  its  circulatory 
activity  and  its  power  of  oxidation.  Such  sweats  do 
nothing  to  remove  the  additive  lactic  acid  from  the 
tissues,  and  so  give  no  relief  to  any  rheumatic  or  other 
symptoms  which  may  be  present.  This  form  occurs 
in  debilitated  subjects.  But  both  classes  are  subject 
to  a  common  danger.  Some  portion  of  the  body  is 
exposed  to  what  is  called  '  a  chill '.  It  means  that  the 
nerves  governing  the  circulation  to  the  capillaries  have 
received  a  shock  which  causes  their  continued  contrac- 
tion over  the  area  affected.  This  condition  may 
continue  for  days  or  weeks,  most  generally  without  the 
patient  being  conscious  of  it,  but  it  can  be  determined 
by  examination,  and  becomes  more  noticeable  when 
the  temperature  of  the  body  is  raised,  when  the  patient 
will  complain  of  '  coldness '  in  this  particular  part. 

The  first  effect  of  the  chill  is  that  lactic  acid  is  not 
excreted  by  the  skin,  and  some  portion  of  it  combines 
with  the  cell- walls  of  the  tissue.  If  there  is  a  reaction, 
the  patient  may  within  twenty-four  hours  complain  of 
tenderness  over  the  part  and  pain  on  movement.  We 
then  connect  the  condition  with  the  word  'rheumatism'. 
But  the  reaction  does  not  always  occur,  or  may  be 
delayed  for  weeks,  when  some  physical  cause,  such  as 
a  sudden  rise  of  temperature  of  the  body,  may  excite 
it ;  or  under  favourable  circumstances  the  whole  con- 
dition may  slowly  return  to  normal  without  the  patient 
being  conscious  of  what  has  taken  place. 

But  a  chill  may  be  general  and  involve  the  whole 
body.  This  checks  the  excretory  action  of  the  skin, 
and  a  large  amount  of  lactic  acid  finds  its  way  to  the 


LACTIC-ACID    DIATHESIS  97 

cell-walls  of  the  tissues.  The  symptoms  presented  will 
depend  on  whether  a  reaction  takes  place  or  not.  In 
the  absence  of  any  reaction,  the  patient  will  complain 
of  feeling  muscularly  tired ;  he  will  have  all  the 
secondary  symptoms  of  over-fatigue  without  having 
done  anything  to  occasion  it.  There  will  be  indisposi- 
tion to  exertion,  but  if  he  should  be  forced  to  take 
exercise,  he  will  feel  rather  better  instead  of  worse  for 
it.  This  distinguishes  it  from  true  debility.  There  is 
often  great  mental  depression,  and  in  severe  cases  it 
may  almost  amount  to  melancholia.  Such  cases  are 
met  with  frequently  in  practice,  and  are  usually  treated 
as  'neurasthenia'.  Unless  something  happens  to  set 
up  a  reaction,  this  condition  may  continue  for  an 
indefinite  period. 

Of  course  there  is  a  marked  variation  in  the  degree 
to  which  patients  suffer  from  these  symptoms.  We 
may  have  anything  from  a  general  indisposition  to 
exertion  to  a  profound  depression  ending  in  suicide. 
Reaction  may  take  place  within  twenty-four  hours  of 
the  chill,  or  be  delayed  for  weeks  or  months,  when  some 
agency  other  than  the  original  chill  sets  it  up.  It  may 
be  an  ordinary  'cold',  exposure  to  heat,  or  an  attack  of 
influenza.  Any  condition  which  raises  the  body  tem- 
perature may  produce  the  reaction. 

Lactic  acid  may  be  regarded  as  matter  in  a  state  of 
incomplete  combustion,  and  once  rapid  oxidation  takes 
place,  as  during  fever,  a  high  temperature  results. 
Given  an  excess  of  lactic  acid  in  the  tissues,  we  are 
likely  to  have  a  high  temperature,  and  usually  accom- 
panied by  very  free  cutaneous  excretion  of  a  very 
acid  character.  Such  cases  may  run  a  course  of  a  few 
days  or  a  few  \veeks,  the  only  symptoms  present  being 
the  temperature  and  the  sweating.  The  more  moderate 

7 


98  RHEUMATISM    AND -THE 

both  symptoms  are,  the  longer  the  condition  may  last. 
Such  cases  are  usually  diagnosed  as  'influenza',  but 
when  they  continue  for  a  long  time  the  diagnosis  may 
be  changed  to  'typhoid',  and  sometimes  they  out-run 
the  temperature  duration  of  this  diagnosis.  I  have 
been  called  in  consultation  to  cases  of  this  kind  which 
have  puzzled  the  physicians  attending. 

There  is  one  symptom  which  I  have  observed  in 
almost  every  case  :  the  pulse  is  not  as  rapid  as  the 
temperature  would  lead  one  to  expect,  and  is  much 
slower  than  in  a  case  where  inflammation  exists.  There 
is  also  an  intensely  acid  reaction  of  the  skin.  The 
explanation  of  these  cases  becomes  very  simple  when 
the  symptoms  are  accompanied  by  swelling  and  inflam- 
mation of  the  joints.  Then  no  one  is  in  doubt  as  to 
the  nature  of  the  diagnosis — -it  is  recognized  as  acute 
rheumatism.  We  see  then  that  a  healthy  man  who 
has  an  excessive  production  of  lactic  acid  is  liable  to 
a  number  of  conditions  all  due  to  the  same  cause,  and 
which  receive  different  names  because  the  symptoms 
differ. 

Many  years  ago  I  called  attention  to  the  importance 
of  the  reaction  of  the  skin  as  a  diagnostic  symptom. 
A  physician  present  at  the  meeting  sent  for  some  blue 
litmus  paper  and  tested  his  own  skin.  The  reaction 
was  intensely  acid.  He  then  produced  the  paper  and 
stated  that  he  had  never  been  in  better  health  in  his 
life.  He  was  under  the  impression  that  this  was  a 
conclusive  argument  against  my  view  Some  years 
later,  I  found  myself  seated  next  this  physician  at  a 
dinner,  and  he  told  me  that  he  had  been  out  of  practice 
for  over  twelve  months  from  a  severe  attack  of  'rheu- 
matic gout'.  Clinical  evidence  in  respect  to  rheumatism 
and  gout  can  only  be  based  on  the  life-history  of  cases 


LACTIC-ACID    DIATHESIS  99 

because  the  removal  of  symptoms  is  no  evidence  of 
cure,  and  the  accession  of  symptoms  or  the  aggravation 
of  those  existing  during  the  attacks  is  often  the  best 
evidence  that  good  results  are  being  obtained.  It  is 
the  condition  of  the  patient  months  or  years  later  that 
gives  us  the  only  evidence  we  can  rely  upon. 

Having  diagnosed  the  case  as  acute  rheumatism, 
because  the  fever,  the  joint  symptoms,  and  the  acidity 
of  the  skin  clearly  point  to  it,  we  shall  regard  this  as  a 
reaction  designed  to  relieve  the  body  of  the  acid  which 
saturates  the  tissues.  Bmt  we  are  taught  not  to  take 
this  view.  On  referring  to  Sajous'  Encyclopaedia  of 
Medicine,  I  find  (p.  479)  that  "  the  conception  of  the 
nature  and  origin  of  the  disease  has,  however,  com- 
pletely changed  during  the  last  decennium.  It  is  now 
commonly  considered  an  infectious  disease.  This  view 
is  based  mainly  upon  the  fact  that  rheumatic  fever  is 
an  epidemic  disease,  and  that  during  epidemics  the 
cases  accumulate  in  some  houses,  whereas  other  houses 

are  quite  spared Although  it  is  commonly 

admitted  that  rheumatic  fever  is  caused  by  an  infectious 
micro-organism,  it  has  not  yet  been  possible  to  discover 
the  specific  microbe  ". 

The  only  claim  advanced  to  prove  rheumatic  fever 
an  infectious  disease  is  that  of  clinical  experience, 
and  this  experience  is  one  of  epidemics  of  rheumatic 
fever.  For  thirty  years  I  have  been  examining  patients 
from  all  parts  of  Great  Britain  who  have  had  attacks 
of  rheumatic  fever,  but  I  have  never  yet  met  with  one 
who  contracted  the  fever  during  an  epidemic  of  the 
disease.  I  have  never  had  any  personal  opportunity 
of  observing  an  epidemic  of  rheumatic  fever,  and  I  am 
not,  therefore,  prepared  to  assert  that  such  a  thing  is 
impossible.  On  the  contrary,  just  as  at  certain  seasons 


100  RHEUMATISM    AND    THE 

of  the  year  and  under  certain  climatic  conditions  we 
have  epidemics  of  influenza,  so  at  a  particular  season 
of  each  year  we  have  the  largest  number  of  cases  of 
acute  rheumatism.  This  season  is  when  the  damp  and 
cold  of  winter  give  place  to  the  more  genial  atmosphere 
of  spring.  The  temperature  of  the  air  rises  rapidly, 
and  at  this  time  acute  rheumatic  complaints  become 
more  prevalent,  so  that  we  find  that  April,  May,  and 
June  are  the  months  when  we  expect  to  see  most  such 
cases.  This  is  clearly  not  due  to  infection,  but  because 
during  the  cold  months  of  the  year  the  excretion  of 
lactic  acid  is  less  active,  and  a  large  quantity  is  locked 
up  in  the  tissues,  and  a  sudden  rise  of  the  temperature 
of  the  air  tends  to  set  it  free  and  produce  symptoms. 

Another  possible  exciting  cause  is  the  bacillus  of 
influenza.  In  respect  to  this  we  know  that  periodically 
we  have  an  infectious  disorder  prevalent.  It  is  not  a 
new  thing,  because  Hippocrates  described  it  some 
centuries  before  the  Christian  era,  and  attributed  the 
disorder  to  climatic  influences.  We  know  that  each 
epidemic  has  its  own  characteristic  symptoms,  and 
these  may  be  of  a  very  varied  character.  We  have  had 
epidemics  when  the  symptoms  nearly  approached  those 
of  dengue  fever,  others  when  pneumonia  has  been  a 
frequent  result,  also  epidemics  causing  temporary 
nephritis,  others  where  eruptions  resembling  scar- 
latina and  measles  were  marked  symptoms ;  but 
more  generally  we  have  cases  where  the  upper  air- 
passages  are  affected  and  pyrexia  is  mild  or  absent. 
We  must  infer  from  this  that  either  there  are  different 
'influenza'  bacilli,  or  that  new  bacilli  of  a  mixed 
character  are  created,  or  that  the  influenza  bacillus 
has  the  power  of  breaking  down  the  resistance  to  other 
bacilli  which  may  exist  in  the  organism  at  the  moment 


LACTIC-ACID    DIATHESIS  101 

of  the  attack.  These  are  questions  which  must  be 
answered  by  the  bacteriologist.  Clinically,  we  have  the 
fact  that  if  we  examine  swabs  from  the  throats  of  a 
number  of  healthy  persons,  we  may  find  the  diphtheria 
bacillus,  the  pneumococcus,  Bacillus  coli,  streptococcus, 
staphylococcus,  etc.  Each  one  of  them  is  capable  of 
producing  symptoms  more  or  less  serious,  but  fails  to 
do  so  because  of  the  resistance  offered  by  the  organism. 
In  dealing  with  cases  of  the  lactic-acid  diathesis 
these  points  are  very  important.  One  of  the  most 
common  symptoms  met  with  in  such  cases  is  a  mild 
chronic  pharyngitis,  with  some  elevation  of  the  papillae 
and  slight  congestion.  This  symptom  passes  unnoticed, 
and  the  only  symptom  produced  is  the  tendency  to 
hawk  up  mucus,  and  'clear  the  throat'.  In  cases  where 
there  is  great  debility  we  may  find  a  membrane  over 
the  back  of  the  pharynx  which  closely  resembles  that 
of  diphtheria.  It  occasions  no  alarm  because  it  is  not 
accompanied  by  any  constitutional  disturbance.  But'A 
patients  with  the  lactic-acid  diathesis  are  very  liable 
to  acute  inflammatory  affections  of  the  tonsils,  accom- 
panied by  a  high  temperature.  The  attack  may  take  -' 
the  form  of  follicular  tonsillitis,  and  in  this  case  its 
diagnosis  presents  no  difficulty.  If,  however,  the 
practitioner  is  anxious  to  avoid  any  mistake,  and  takes 
a  swab  and  sends  it  to  a  bacteriological  laboratory,  he 
will  very  likely  be  informed  that  the  diphtheria  bacillus 
is  present  and  the  case  is  one  of  diphtheria.  He  will 
therefore  feel  bound  at  once  to  administer  antitoxin, 
although  all  the  clinical  symptoms  are  those  of  follicu- 
lar tonsillitis.  But  when  the  tissues  are  charged  with 
lactic  acid  they  are  very  intolerant  to  antitoxin,  and 
in  such  cases  it  is  likely  to  cause  serious  irritation 
of  the  kidney  or  inflammatory  affections  of  the  skin. 


vl    h 

r-K\  t; 


102  RHEUMATISM    AND    THE 

These  cases  clear  up  rapidly  when  a  solution  of 
biniodide  of  mercury  is  applied  to  the  tonsils  and 
pharynx.  I  use  i  gr.  of  the  biniodide  to  4  oz.  of  water, 
with  a  few  grains  of  potassium  iodide  added  to  effect 
solution.  A  small  quantity  of  this  is  sprayed  or  painted 
on  the  tonsils  every  three  hours.  Immediately  before 
the  application  is  made  I  add  10  drops  of  peroxide 
of  hydrogen  to  the  portion  of  the  solution  to  be  used. 
This  causes  decomposition,  and  the  solution  is  used  in 
a  nascent  form  which,  I  think,  adds  to  its  efficiency. 

The  whole  question  has  been  complicated  by  the 
insistence  on  the  view  that  rheumatic  fever  is  itself  an 
infectious  disease.  Its  relation  to  inflammatory  affec- 
tions of  the  tonsils  has  led  to  the  theory  that  it  is  by 
the  tonsils  and  pharynx  that  it  gains  admission  to  the 
body.  If  we  accept  this  view,  we  must  suppose  that  a 
health}7  man  is  liable  to  become  infected  with  rheu- 
matism, and  that  rheumatic  fever  is  the  expression 
and  natural  result  of  that  infection.  We  cannot  explain 
how  he  becomes  infected.  The  rheumatic-fever  patient 
has  never  been  known  to  infect  any  other  person.  This 
difficulty  has  been  got  over  by  explaining  that  the 
bacilli  are  too  deep  in  the  joints  to  infect  other  persons. 

Such  arguments  betray  a  great  lack  of  knowledge  of 
the  clinical  symptoms  of  acute  rheumatism.  Beyond 
all  other  diseases,  rheumatic  fever  is  a  disorder  attended 
by  the  excretion  of  the  poison  which  causes  the  disease. 
When  that  excretion  is  finished — and  we  know  when  by 
the  return  of  the  reaction  of  the  skin  to  normal — all 
the  symptoms  subside  and  the  patient  recovers.  The 
bacilli  cannot  remain  deep  down  in  the  joints  under 
such  conditions. 

If  we  examine  the  history  of  any  patient  previous 
to  the  attack  of  rheumatic  fever,  we  shall  invariably 


LACTIC-ACID    DIATHESIS  10:; 

obtain  evidence  that  for  weeks  before  the  attack  he 
suffered  from  some  of  the  symptoms  I  have  already 
described.  Many  years  ago  I  gave  the  name 
'asthenoxia'  to  this  condition.  It  may  not  prevent  a 
man  doing  his  work,  but  he  does  it  as  a  tired  man,  and 
keeps  going  by  effort.  When  rheumatic  fever  is 
properly  treated,  the  malaise  is  the  first  symptom  to 
disappear. 

The  bacteriological  theory  of  rheumatic  fever  is 
wholly  unnecessary  to  explain  any  single  symptom  of 
the  disease,  and  raises  questions  which  it  is  impossible 
to  answer.  It  causes  confusion  of  thought  on  a  matter 
which,  in  every  detail,  is  otherwise  simple  and  intelligible. 
But  just  as  we  have  sporadic  cases  of  diphtheria  and 
diphtheria  as  an  infectious  disease,  so  it  is  alleged  that 
we  have  epidemics  of  rheumatic  fever  and  that  it  assumes 
an  infective  form.  I  have  no  personal  knowledge  of 
such  epidemics,  but  I  can  easily  imagine  the  conditions 
.under  which  they  could  occur. 

Take  a  community  who  earn  their  living  by  hard 
physical  exertion,  involving  strain  upon  the  joints  and 
tendons.  We  have  only  to  suppose  a  period  of  cold 
and  damp  weather  when  the  excretion  of  the  skin  is 
inactive,  followed  by  a  mild  attack  of  influenza  which 
raises  the  temperature  of  the  body,  for  all  the  symptoms 
of  rheumatic  fever  to  be  set  up  in  a  considerable  number 
of  people  at  the  same  moment. 

If  the  bacillus  happened  to  be  that  of  scarlatina,  the 
result  would  be  the  same.  Any  bacillus,  or  any  physical 
cause  which  would  suddenly  raise  the  temperature  of 
the  body  under  such  conditions,  would  be  sufficient  to 
set  up  either  rheumatic  fever  or  a  high  temperature 
without  joint  symptoms.  As  a  matter  of  fact  we  see 
such  cases  during  every  epidemic  of  influenza  ;  but  if 


104  RHEUMATISM    AND    THE 

the  joint  symptoms  appear  we  call  it  rheumatic  fever, 
and  if  there  are  no  joint  symptoms  we  regard  it  as  a 
severe  attack  of  influenza.  But  other  persons  in  the 
same  house,  infected  by  the  same  bacillus,  will  show  a 
very  slight  rise  of  temperature,  which  may  subside  in 
twenty-four  to  thirty-six  hours.  No  clearer  proof 
could  be  given  that  the  patient  who  has  the  high 
temperature,  lasting  perhaps  for  two  or  three  weeks  or 
longer,  has  some  underlying  condition  which  makes  the 
symptoms  he  presents  altogether  different  from  those 
exhibited  by  other  patients. 

It  is  well  known  that  some  of  these  cases  make  a 
rapid  convalescence  after  an  attack  of  high  fever ; 
others  may  remain  debilitated  for  months  afterwards. 
It  is  not  difficult  to  give  an  accurate  prognosis  as 
to  which  result  is  likely  to  happen.  If  we  take  the 
reaction  of  the  skin  during  the  attack,  we  shall 
find  that  it  is  extremely  acid.  This  is  invariably  the 
case  unless  the  excretion  of  the  skin  is  arrested,  and 
this'rarely  occurs.  If  we  watch  the  reaction  of  the  skin, 
and  find  that  it  remains  intensely  acid  for  some  days 
after  the  temperature  has  fallen,  we  can  predict  a 
prolonged  convalescence.  If  the  acid  reaction  of  the 
skin  diminishes  as  the  temperature  falls,  we  can  say 
with  certainty  that  the  patient  will  make  a  rapid 
recovery.  It  is  many  years  since  I  first  described  this 
prognostic  symptom,  and  I  have  never  known  it  to 
fail. 

But  when  the  acid  condition  remains  after  the  tem- 
perature has  fallen,  I  do  not  give  an  unfavourable 
prognosis,  because  I  take  immediate  steps  to  carry  on 
the  work  which  nature  has  failed  to  accomplish.  I 
will  explain  this  method  in  the  chapter  on  '  Pyretic 
Treatment '.  The  point  I  am  anxious  to  insist  upon 


LACTIC-ACID    DIATHESIS  105 

is  that  in  most  cases  where  there  is  prolonged  con- 
valescence from  'influenza',  there  exists  an  excess  of 
lactic  acid  in  the  cell-walls  of  the  patient's  tissues,  and 
if  proper  means  are  taken  to  remove  this,  they  will 
ensure  a  rapid  recovery.  It  is  for  this  reason  that 
tonic  remedies  fail  in  such  cases.  The  cause  is  practi- 
cally physical,  and  only  physical  methods  can  assure 
good  results. 

I  will  deal  with  the  symptoms  of  chronic  rheumatism 
in  the  chapter  on  'Arthritis',  not  because  the  term 
should  ever  be  applied  to  it,  but  because  it  will  be 
a  more  convenient  place  to  discuss  its  differential 
diagnosis  from  'rheumatoid  arthritis',  with  which  it  is 
commonlv  confused. 


106 


CHAPTER    VIII. 

RHEUMATIC    FEVER. 

IN  a  typical  case  of  rheumatic  fever  there  are  practically 
three  distinct  symptoms :  (i)  The  fever ;  (2)  The 
inflammation  of  the  joints  ;  (3)  The  acid  excretion  of 
the  skin. 

We  see  a  large  number  of  cases  where  only  the  second 
symptom  exists.  There  is  an  inflammatory  condition  of 
the  joints,  accompanied  by  pain,  but  there  is  no  fever 
and  no  excessive  excretion  by  the  skin  ;  this,  in  fact, 
may  be  altogether  arrested.  We  know  that  in  rheumatic 
fever,  within  a  certain  number  of  days  or  weeks  the 
attack  will  come  to  a  termination,  under  any  kind  of 
treatment  ;  that  in  the  case  unattended  by  fever  it 
may  go  on  for  years  and  increase  rather  than  decrease 
in  severity.  This  teaches  us  to  regard  the  fever  and 
acid  sweats  as  symptoms  of  active  metabolism  rather 
than  as  symptoms  of  disease.  It  is  because  this  lesson 
has  never  been  learned  that  a  clinical  experience  has 
been  created  which  conveys  the  idea  that  rheumatic 
fever  is  a  disease  in  which  relapse  is  very  frequent, 
convalescence  is  prolonged,  and  over  70  per  cent  of 
cases  are  left  with  valvular  disease  of  the  heart. 

The  physiological  studies  which  I  have  recorded 
enable  us  to  understand  clearly  why  these  results 
happen,  and  the  method  by  which  they  can  be  avoided. 
We  know  that  every  patient  who  suffers  from  rheumat it- 
fever  has,  prior  to  the  attack,  a  large  amount  of  additive 
lactic  acid  in  the  cell-walls.  We  know  from  our  experi- 


RHEUMATIC    FEVER  107 

ments  that  the  tissues  are  capable  of  taking  up  a  large 
amount  of  lactic  acid  beyond  that  which  is  necessary 
to  combine  with  the  phosphate  of  lime  in  the  cell-walls, 
and  this  addition  makes  no  difference  to  the  chemical 
combination  of  lactophosphate  of  lime,  nor  does  it 
alter  its  crystalline  form  ;  but  the  additive  lactic 
acid  is  in  such  close  cohesion,  that  it  is  uninfluenced 
by,  nor  does  it  influence,  alkaline  fluids  surrounding  it. 
But  when  a  rise  of  temperature  takes  place,  some 
portion  of  the  additive  lactic  acid  is  set  free,  and  the 
process  continues  during  the  whole  period  of  the  fever. 
We  know,  therefore,  that  the  patient  has  been  exposed 
to  certain  conditions  which  either  increase  the  produc- 
tion of  lactic  acid  or  have  checked  its  elimination. 

As  regards  increased  production,  we  know  that  there 
are  three  factors  concerned,  acting  either  in  conjunction 
or  singly  '•  (i)  Increased  muscular  action  ;  (2)  Exhaus- 
tion of  the  nerve-supply  ;  (3)  Imperfect  oxidation,  from 
alteration  in  the  quantity  or  quality  of  the  blood-supply. 
It  is  important  to  determine  these  factors  in  every  case, 
with  a  view  to  placing  the  patient  under  such  conditions 
as  will  prevent  this  excessive  production. 

As  regards  the  defect  in  its  elimination,  we  have  to 
consider  the  causes  which  check  the  normal  functional 
activity  of  the  skin  or  which  prevent  the  oxidation  of 
lactic  acid  in  the  tissues.  Exposure  to  cold  and  damp 
are  common  factors  in  producing  this  condition,  and 
deficiency  of  haemoglobin  in  the  blood  is  another  factor 
found  in  a  certain  proportion  of  cases.  There  is  no 
evidence  to  show  that  lactic  acid  is  destructive  to  the 
haemoglobin  ;  but  the  absence  of  haemoglobin  is  favour- 
able to  the  presence  of  an  excess  of  lactic  acid. 

We  have  already  dealt  with  the  symptoms  which 
may  occur,  due  to  this  condition,  prior  to  the  attack 


108  RHEUMATIC    FEVER 

of  rheumatic  fever.  The  immediate  cause  of  the  actual 
attack  is  any  factor  which  may  bring  about  a  sudden 
rise  of  the  temperature  of  the  body.  It  may  be  a 
reaction  from  a  chill,  the  presence  of  any  bacillus,  or 
the  result  of  any  physical  condition  which  causes  a 
temporary  pyrexia.  In  my  experiments  with  animal 
tissues  saturated  with  lactic  acid,  I  have  shown  that  a 
rise  of  temperature  liberates  the  additive  lactic  acid. 
I  have  further  demonstrated  that  the  presence  of  free 
lactic  acid  prevents  urea  from  combining  with  chloride 
of  sodium  to  form  the  urate,  that  lactic  acid  combines 
instead  with  the  urea,  to  form  lactate  of  urea,  and  this 
passes  quickly  into  lactate  of  ammonia.  In  this  way 
the  alkalinity  of  the  tissues  is  preserved. 

But  lactic  acid  cannot  combine  with  ammonia  without 
the  evolution  of  heat.  If  we  add  lactic  acid  drop  by 
drop  to  a  solution  of  ammonia,  we  can  maintain  the 
temperature  of  the  mixture  for  an  indefinite  period. 
When  the  tissues  are  saturated  with  lactic  acid,  as  they 
are  at  the  moment  of  the  attack  of  rheumatic  fever, 
the  quantity  of  lactic  acid  liberated  by  a  small  rise  of 
temperature  will  be  sufficient  to  raise  the  body  tempera- 
ture to  a  still  higher  level,  and  this  in  turn  will  liberate 
more  lactic  acid,  so  that  a  further  rise  of  temperature 
takes  place ;  and  this  will  continue  until  a  balance  is 
established  between  the  rate  of  liberation  of  the  lactic 
acid  and  the  temperature  reached,  because  as  soon  as 
the  excess  of  additive  lactic  acid  is  removed,  the  rate 
of  liberation  is  diminished.  This  will  explain  how  it 
happens  that  the  temperature  in  rheumatic  fever  almost 
invariably  rises  by  stages  to  a  certain  level,  and  is  then 
maintained  at  that  level  with  small  fluctuations  over 
an  indefinite  period. 

The  chemical  nature  of  the  fever  is  indicated  by  the 


RHEUMATIC    FEVER  109 

fact  that  the  pulse-rate  is  not  under  normal  conditions 
increased  to  the  same  amount  as  would  happen  if  the 
fever  were  the  result  of  inflammation.  When  a  rapid 
pulse  occurs  under  such  conditions,  we  can  be  sure  that 
the  heart  is  being  irritated  by  the  failure  of  the  organism 
to  neutralize  the  lactic  acid.  This  result  is  most  likely 
to  occur  if  the  normal  functions  of  the  body  are  inter- 
fered with  by  the  ill-advised  use  of  certain  drugs.  The 
whole  treatment  of  rheumatic  fever  must  be  based  upon 
the  point  of  view  from  which  we  regard  the  temperature. 

That  fever  is  a  pathological  symptom  has  been  taught 
by  the  physicians  of  all  ages.  Even  at  the  present  day 
the  chief  use  made  of  the  thermometer  is  to  detect  fever 
as  a  pathological  symptom.  I  have  found  physicians 
who  could  not  understand  the  reason  for  taking  the 
temperature  of  patients  two  or  three  times  a  day  when 
no  fever  existed.  The  enormous  importance  of  the 
subnormal  temperature  has  never  been  fully  realized, 
because  nurses  do  not  always  shake  the  index  of  the 
thermometer  to  95°  before  they  take  a  patient's 
temperature,  and  many  temperature  charts  do  not 
afford  any  space  for  these  low  temperatures. 

In  the  treatment  of  all  disorders  of  metabolism,  the 
temperature,  whether  it  is  high  or  low,  affords  us  the 
best  chemical  indication  we  can  have  of  the  chemical 
activities  of  the  body. 

We  must  begin  by  discarding  the  idea  that  a  rise  of 
temperature  above  normal  is  of  necessity  a  pathological 
symptom.  This  is  easily  demonstrated  by  the  fact 
that  no  healthy  person  can  take  active  exercise  without 
producing  a  rise  of  temperature.  We  know  that  exer- 
cise increases  the  production  of  lactic  acid.  lit  is 
probable  that  the  rise  of  temperature  of  the  body  is  in 
large  part  due  to  the  excess  of  lactic  acid  produced 


110  RHEUMATIC    FEVER 

during  exercise :  even  healthy  people  have  some 
additive  lactic  acid  in  the  cell-walls,  and  this  is  liberated 
during  exercise.  I  think  this  conclusion  is  correct, 
because  the  man  who  takes  active  exercise  daily  does 
not  develop  the  same  amount  of  heat  as  a  result  of  any 
specific  act  of  exertion  as  the  man  of  sedentary  habits 
who  takes  active  exercise  occasionally.  We  may  account 
for  this  by  the  fact  that  the  man  of  sedentary  habits  has 
a  larger  amount  of  additive  lactic  acid  in  his  cell-walls. 

I  have  found  some  physicians  so  impressed  by  the. 
heat-regulating  mechanism  of  the  body  that  they  have 
doubted  whether  exercise  does  produce  a  rise  of 
temperature.  A  medical  friend  disputed  this  point 
one  night.  The  next  day  he  met  me  and  admitted  that 
I  was  right.  He  told  me  that  he  had  used  the  mowing- 
machine  on  his  lawn,  with  a  thermometer  in  his  mouth. 
The  heat-regulating  mechanism  of  the  body  would  be 
more  effective  if  we  did  not  happen  to  wear  clothes. 

The  fever  of  rheumatic  fever  is  as  much  a  physio- 
logical process  as  the  fever  due  to  active  exercise,  and 
is  due  to  precisely  the  same  chemical  activities.  It  was 
the  study  of  rheumatic  fever  which  first  led  me  to 
understand  that  fever  may  be  a  normal  physiological 
process,  and  also  a  very  powerful  therapeutic  agent. 
When  I  brought  forward  this  view  at  a  medical  society 
some  twenty  years  ago,  almost  all  my  auditors  thought 
it  necessary  to  give  their  reasons  for  dissenting  from 
this  proposition.  But  within  a  few  months,  without 
any  further  arguments  from  myself,  many  of  these,  on 
reflection,  came  to  the  conclusion  that  the  view  was 
sound.  At  the  time  I  was  not  in  a  position  to  arrive 
at  my  conclusions  by  induction,  and  had  to  depend  upon 
deduction.  Whichever  method  we  employ  the  result 
is  the  same. 


RHEUMATIC    FEVER  111 

The  view  that  the  fever  was  a  pathological  symptom 
led  to  methods  of  treatment  that  would  most  quickly 
cure  the  fever,  and  the  discovery  of  salicylic  acid  and 
its  salts  was  hailed  with  great  enthusiasm.  It  was 
necessary  to  give  the  drug  in  large  doses  to  produce  the 
result.  Under  its  influence  the  fever  subsided  and  the 
pain  and  inflammation  of  the  joints  was  relieved,  so 
that  the  patient  was  comparatively  quickly  able  to  be 
removed  from  the  hospital.  But  from  the  Reports  of 
St.  Bartholomew's  Hospital  (Dr.  Samuel  West,  Prac- 
titioner, 1888,  p.  104),  70  to  86  per  cent  of  the  patients 
treated  developed  heart  disease  as  a  result  of  the  attack. 

Xot  only  is  heart  disease  regarded  as  an  after-result 
from  which  few  escape,  but  also  prolonged  convalescence 
and  relapse  are  regarded  as  essential  clinical  symptoms 
of  the  disease.  Thirty  years'  experience  in  the  treatment 
of  rheumatic  fever  and  its  after-results  enables  me  to 
state  positively  that  these  clinical  results  are  due 
almost  in  their  entirety  to  a  false  conception  of  the 
nature  of  the  disease  and  to  the  efforts  to  suppress  the 
normal  physiological  reactions  intended  to  avert  these 
dangers.  If  rheumatic  fever  is  not  interfered  with  by 
drugs  or  any  agents,  it  will  run  its  course  in  a  certain 
number  of  weeks,  and  both  the  fever  and  the  joint 
symptoms  will  disappear.  In  a  case  of  chronic  rheu- 
matism we  have  the  same  joint  symptoms,  but  fever 
is  absent,  and  the  condition  may  continue  for  years, 
and  there  is  no  tendency  to  natural  recovery.  It  might 
be  thought  that  these  clinical  facts  alone  would  have 
made  it  clear  that  the  arrest  of  the  fever  in  rheumatic 
fever  might  have  dangerous  consequences  ;  but  in  spite 
of  the  very  serious  results  which  have  followed  the  use 
of  salicylates  and  similar  remedies,  they  have  con- 
tinued to  be  employed. 


112  RHEUMATIC    FEVER 

The  real  problem  in  the  cure  of  rheumatism  is  to 
find  some  agent  which  will  liberate  the  additive  lactic 
acid  from  the  cell-wall.  In  my  experiments  with 
animal  tissues  containing  an  excess  of  lactic  acid,  it 
was  shown  that,  if  we  surrounded  the  tissue  with  an 
alkaline  solution,  no  chemical  combination  took  place 
except  when  we  added  sufficient  heat  to  liberate  the 
lactic  acid.  This  is  the  method  of  Nature,  and  I  have 
discovered  no  other. 

From  this  we  might  suppose  that  if  we  left  patients 
without  any  treatment  in  rheumatic  fever  they  would 
make  a  good  recovery.  Unquestionably  they  would 
be  much  better  than  with  the  results  of  salicylate 
treatment ;  but  during  my  long  experience  the  number 
of  patients  I  have  seen  where  Nature  brought  the  case 
to  a  satisfactory  conclusion  is  very  limited. 

One  case  occurred  in  my  early  experience.  A  robust 
girl,  18  years  of  age,  developed  rheumatic  fever.  She 
had  a  very  high  temperature,  all  the  joints  of  the  limbs 
were  involved,  there  was  profuse  acid  sweating,  con- 
tinued acid  vomiting,  and  a  diarrhoea  which  consisted 
chiefly  of  a  large  amount  of  acid  fluid.  In  this  case  I 
merely  gave  a  placebo  ;  no  help  appeared  necessary. 
The  patient  made  a  good  recovery  in  three  weeks,  and 
has  remained  without  any  further  attack  for  thirty  years. 
The  patient  was  of  the  well-marked  lactic-acid  diathesis, 
and  her  mother  and  grandmother  both  had  valvular 
disease  of  the  heart  as  a  result  of  rheumatic  fever. 

In  a  number  of  cases  the  physiological  reactions 
are  sufficient  in  the  early  stages,  and  only  need  help  if 
the  skin  should  be  inactive,  as  sometimes  happens  ; 
but  there  comes  a  time  when  the  temperature  falls 
and  the  patient  appears  to  be  approaching  recovery. 
This  is  the  most  critical  stage  in  the  treatment  of 


RHEUMATIC    FEVER  113 

rheumatic  fever.  If,  in  spite  of  the  fall  of  temperature, 
the  reaction  of  the  skin  remains  very  acid,  even  if  the 
joint  symptoms  have  subsided,  we  can  be  sure  that 
the  patient  will  have  a  prolonged  convalescence  and 
is  in  danger  of  relapse,  unless  we  take  artificial  means 
to  maintain  the  temperature  and  ensure  the  physio- 
logical activity  of  the  skin.  The  reaction  oi_the  skin 
is  the  one^  clinical  fact  which_must  guide  us  in  these 
cases.  If  we  take  means  to  prolong  the  attack  until 
~tHe  skin  becomes  only  moderately  acid,  we  can  then 
be  sure  that  the  patient  will  have  a  quick  convalescence 
and  be  in  no  danger  of  relapse.  The  method  of  treat- 
ment adopted  will  be  best  considered  in  the  next  chapter. 
The  results  of  treatment  of  rheumatic  fever  when 
properly  carried  out  are  wholly  satisfactory.  Heart 
disease  rarely  occurs  if  the  patient  is  seen  at  an  early 
stage,  and  a  blowing  murmur  frequently  heard  over 
the  heart  on  admission  usually  disappears  in  the  course 
of  treatment.  It  is  quite  common  for  a  patient  with 
rheumatic  fever,  before  the  temperature  and  the  joint 
symptoms  have  subsided,  to  express  himself  as  feeling 
better  than  he  has  felt  for  months.  The  appearance 
of  the  patient  affords  evidence  of  this.  The  com- 
plexion, which  had  the  dull  opaque  appearance  which 
is  significant  of  lactic-acid  excess,  changes,  and  there 
"isfgreater  translucency  of  the  skin.  The  eyes  also  have 
a  brighter  and  clearer  appearance.  These  symptoms 
afford  proof  that  the  fever  has  removed  something 
from  the  tissues  which  was  depressing  their  normal 
physiological  activity. 

Relapse  may_be  said  never  to  occur  in  cases  efficiently 
and completely  treated.  I  emphasize  the  word  'com- 
pletely', because  the  symptoms  of  'cure'  are  often 
misleading.  Thus,  a  healthy-looking  boy  appeared  at 


114  RHEUMATIC    FEVER 

the  out-patient  department  complaining  of  rheumatic 
pains  in  the  muscles  of  the  back.  He  had  been  sleep- 
ing on  the  ground  in  a  boy's  camp.  Now,  as  a  number 
of  boys  were  exposed  to  the  same  conditions,  there 
must  have  been  some  antecedent  condition  existing  in 
the  boy,  as  he  was  the  only  one  who  developed  any 
rheumatic  symptoms.  His  skin  showed  an  extremely 
acid  reaction.  I  attach  very  great  importance  to  this 
symptom  in  children.  The  lactic-acid  diathesis  may, 
in  such  cases,  first  make  its  presence  known  by  some 
permanent  mischief  to  the  valves  of  the  heart,  by 
pericarditis,  endocarditis,  or  pleurisy.  We  may,  of 
course,  have  far  less  urgent  symptoms  as  a  result 
of  the  condition  ;  we  may  have  pains  about  the 
body  which  used  to  be  explained  as  'growing  pains'. 
Because  I  took  the  view  that  this  symptom  should 
be  treated  seriously,  I  ordered  the  boy  into  hospital, 
and  gave  him  treatment  which  consisted  in  causing  an 
artificial  rise  of  temperature  each  day.  On  the  third 
day  he  developed  an  attack  of  rheumatic  fever,  which 
ran  an  ordinary  course  for  three  weeks  and  then  sub- 
sided. The  boy  expressed  himself  as  quite  well,  and 
there  was  nothing  to  prevent  his  discharge  except  that 
the  reaction  of  the  skin  was  almost  as  acid  as  on  the 
day  of  admission.  I  therefore  ordered  the  treatment  to 
be  continued.  Within  forty-eight  hours  the  tempera- 
ture rose  again  and  several  joints' were  inflamed.  This 
continued  for  a  fortnight,  when  the  attack  subsided. 
His  skin  then  showed  very  slight  acidity  and  I  dismissed 
him.  I  had  the  opportunity  of  watching  the  history 
of  the  case  for  ten  years,  and  there  was  no  return  of 
the  slightest  rheumatic  symptom.  He  developed  into 
a  very  healthy  man.  In  this  case,  if  I  had  dismissed 
the  boy  when  the  symptoms  were  'cured',  he  would 


RHEUMATIC    FEVER  115 

most  certainly  have  had  a  relapse  sooner  or  later,  and 
the  relapse  would  have  been  explained  as  the  normal 
character  of  the  disease.  It  would  have  been  really 
due  to  the  fact  that  my  treatment  had  not  been 
complete. 

This  case  emphasizes  not  only  this  point,  but  also 
the  fact  that  even  in  a  healthy  boy  Nature  may  fail  to 
complete  the  reaction,  and,  as  a  matter  of  fact,  does 
fail  to  do  so  in  the  large  majority  of  cases  of  rheumatic 
fever.  It  is  on  this  account  that,  while  we  regard  the 
symptoms  as  physiological  which  it  would  be  wrong  to 
suppress,  almost  every  case  calls  for  active  treatment, 
and  more  especially  in  its  later  stages. 

A  large  number  of  cases  are  sent  to  us  as  cases  of 
rheumatic  fever  where,  after  prolonged  convalescence, 
the  symptoms  of  rheumatism  in  its  more  chronic  form 
have  developed.  In  these  cases  the  treatment  may 
reproduce  the  rheumatism  in  its  acute  form,  and  there 
may  be  a  continued  temperature  for  some  time.  When 
this  occurs,  recovery  occurs  at  an  earlier  date  than 
when  a  rise  of  temperature  only  occurs  during  the 
actual  process  of  treatment.  In  either  case  the  results 
are  always  satisfactory. 

Some  years  ago  a  special  number  of  the  Practitioner 
was  published  in  which  physicians  were  invited  to 
give  their  experience  in  the  treatment  of  rheumatism. 
I  remember  reading  of  a  case  treated  at  the  Glasgow 
Royal  Infirmary  by  'Wilde's  treatment'.  The  hot 
blanket  pack  appears  to  have  been  used  for  raising 
the  patient's  temperature.  Under  this  treatment  the 
patient's  temperature  rose,  and  fresh  joints  became 
implicated.  As  this  continued,  a  consultation  was 
called,  and  it  was  decided  to  abandon  the  treatment. 
Other  methods  were  employed,  and  the  patient  was 


116  RHEUMATIC    FEVER 

finally  dismissed  unimproved.  Some  three  months 
later  the  man  reappeared  at  the  hospital  quite  well. 
On  being  asked  what  he  had  done,  he  said  that  he 
knew  the  treatment  they  started  with  was  doing  him 
good,  so  when  he  went  home  he  got  his  wife  to  con- 
tinue it.  This  case  points  to  the  necessity  of  the 
physician  who  conducts  such  treatment  having  the 
courage  of  his  convictions,  and  always  remembering 
that  neither  the  fever  nor  the  joint  symptoms  are 
pathological. 

Another  misfortune  happens  to  rheumatic-fever 
patients  because  the  fever  is  wrongly  regarded.  It  is 
quite  customary  to  order  a  milk  diet  to  such  patients. 
As  all  the  tissues  are  saturated  with  lactic  acid,  and 
lactic  acid  is  being  excreted  into  the  stomach  and  in- 
testines, milk  happens  to  be  the  one  food  that  is  likely 
to  augment  the  existing  conditions.  As  a  consequence, 
a  thickly-coated '  tongue  with  gastric  disturbance  is 
regarded  as  a  normal  symptom  of  rheumatic  fever. 
With  ordinary  diet,  with  the  exclusion  of  milk  except 
in  small  quantities,  and  with  the  use  of  simple  salines 
to  assist  the  excretion  of  the  intestinal  contents,  these 
symptoms  do  not  occur. 

We  may  divide  rheumatic-fever  cases  into  sthenic 
and  asthenic.  In  the  sthenic  cases  with  high  tempera- 
ture, small  doses  of  acetylsalicylic  acid  at  infrequent 
intervals  will  modify  the  temperature  and  ease  the 
pain,  and  also  promote  the  action  of  the  skin.  There 
is  no  danger  in  the  use  of  this  drug  or  the  salicylates  so 
long  as  they  are  not  used  in  antipyretic  doses.  In  the 
asthenic  cases,  means  to  raise  the  body  temperature 
should  be  employed  from  the  first,  and  as  in  these  cases 
there  is  usually  defective  oxidation,  the  use  of  nitro- 
genous foods  is  indicated  and  assists  the  treatment. 


117 


CHAPTER    IX. 

PYRETIC    TREATMENT. 

THIS  term  applies  to  any  method  which  has  for  its 
object  the  elevation  of  the  temperature  of  the  body 
for  purposes  of  treatment.  It  does  not  include  processes 
in  which  hot  dry  air  is  applied  to  the  body  either 
generally  or  locally,  or  those  in  which  the  aim  is  to 
cause  sweating,  without  regard  to  the  temperature 
of  the  body.  Before  I  discuss  the  technique  of  this 
method,  it  will  be  better  to  point  out  its  therapeutic 
value  and  the  conditions  indicating  it. 

It  was  the  study  of  rheumatism  in  its  acute  and 
chronic  forms  which  first  directed  my  attention  to  the 
value  of  fever  as  a  therapeutic  agent.  Rheumatism 
attended  with  fever  runs  a  definite  course,  and  its 
natural  tendency  is  to  recovery.  Rheumatism  without 
fever  has  no  tendency  to  natural  recovery,  and  may  go 
on  for  years  and  become  progressively  worse.  As  I 
have  shown,  acute  rheumatism  may  drift  into  the 
chronic  condition  as  a  result  of  artificially  suppressing 
the  fever,  or  we  may  have  heart  complication  and 
relapse  from  a  similar  cause. 

The  value  of  fever  in  the  cure  of  rheumatism  is 
demonstrable  by  the  experiments  I  have  described  in 
the  chapter  on  lactic  acid.  When  we  supersaturate 
an  animal  tissue  with  lactic  acid,  and  wash  and  dry 
the  specimen,  we  have  a  tissue  that  will  present  a  very 
acid  reaction  to  blue  litmus  paper,  but  which,  if  placed 
in  an  alkaline  solution,  will  neither  impart  its  acidity  to 


118  PYRETIC    TREATMENT 

the  alkali  nor  become  neutralized  by  the  alkali  in  the 
solution.  I  have  demonstrated  that  this  is  not  due 
to  the  whole  of  the  lactic  acid  being  in  chemical  com- 
bination ;  the  bulk  of  it  is  simply  '  additive '  and  held 
in  a  state  of  cohesion.  I  have  shown  that  this  cohesion 
can  be  overcome  by  raising  the  temperature  of  the 
fluid  in  which  the  acid  tissue  is  placed,  and  that  under 
these  circumstances  the  acid  is  slowly  set  free.  This  ex- 
plains why  alkaline  treatment  of  rheumatism,  even  if 
it  relieves  symptoms  by  combining  with  any  free  acid 
which  may  be  present,  will  fail  to  cure,  because  it  cannot 
liberate  the  acid  in  cohesion  with  the  tissues.  The 
production  of  fever  is  the  method  adopted  by  Nature, 
and  so  far  I  have  not  been  able  to  discover  any  other 
method  which  will  accomplish  the  same  result. 

There  are  many  ways  in  which  the  temperature  of 
the  body  can  be  artificially  raised.  It  is  not  dependent 
upon  any  particular  form  of  apparatus,  although  I 
have  designed  some  as  a  matter  of  efficiency  and  con- 
venience. In  1893  I  published  the  results  of  five  years' 
use  of  pyretic  treatment  (Rheumatism,  Bale  &  Sons), 
and  described  a  simple  appliance  I  had  designed  for 
use  in  rheumatic  fever.  This  was  at  once  'improved' 
upon  for  commercial  purposes,  and  this  in  turn  was  still 
further  improved  upon  by  other  inventors,  whose  aim 
appeared  to  be  to  submit  the  body  to  very  high  tem- 
peratures, and  these  appliances  have  been  used  all  over 
the  world.  The  result  has  been  that  the  true  object  of 
the  appliance  I  used  has  been  completely  misunderstood, 
and  a  method  of  treatment  adopted  which  has  many 
grave  disadvantages.  It  is  for  this  reason  that  it  is 
necessary  for  me  to  trouble  the  reader  with  some 
elementary  physiological  facts. 

The  human  body  is  a  heat-producing  machine,  and 


PYRETIC    TREATMENT  119 

radiates  heat.  To  apply  a  very  high  temperature  to 
the  human  body  we  must  employ  dry  air.  If  we  used 
water  or  steam,  we  should  burn  the  skin  at  a  much 
lower  temperature,  because  the  vehicle  we  employed 
would  check  the  heat  radiation  from  the  body.  Hot 
dry  air  does  not  do  so  because  it  assists  the  radiation 
of  heat.  Thus  the  nude  man  in  the  hottest  room  of  a 
Turkish  bath  will  have  a  normal  temperature.  I  say 
nothing  about  the  dilatation  of  the  blood-vessels  favour- 
ing the  radiation  of  heat,  because  this  takes  place  with 
all  forms  of  heat. 

In  order  to  raise  the  body  temperature,  we  are  only  \ 
concerned  with  methods  which  check  the  radiation 
of  heat  from  the  body,  and  those  which  increase  its 
production.  But  if  we  check  the  radiation  of  heat 
from  the  body  and  raise  the  temperature,  without  se- 
curing dilatation  of  the  cutaneous  blood-vessels  and  the 
consequent  action  of  the  sweat-glands,  we  induce  a  con- 
dition of  congestion,  which  will  be  followed  by  malaise, 
because  we  have  set  free  acid  from  the  tissues  without 
securing  its  elimination.  Thus,  if  we  take  a  man  with 
dry  inactive  skin,  and  wrap  him  in  a  number  of  blankets, 
we  can  secure  a  rise  of  temperature  of  the  body  ;  but 
if  no  action  of  the  skin  takes  place,  he  suffers  from 
congestion,  which  will  be  only  relieved  as  the  acid  set 
free  is  eliminated  by  the  lymphatics. 

For  this  reason,  when  we  raise  the  body  temperature, 
it  is  necessary  to  use  such  a  degree  of  heat  as  will  dilate 
the  blood-vessels  and  secure  cutaneous  excretion.  It 
is  at  this  point  that  confusion  of  thought  occurs.  It 
appears  to  many  that  any  method  which  secures  free 
cutaneous  excretion  is  sufficient,  and  that  this  is  the 
mode  of  treatment  indicated.  But  we  can  obtain  free 
excretion  of  the  skin  by  hot  dry  air,  as  in  the  Turkish 


120  PYRETIC    TREATMENT 

bath,  without  raising  the  body  temperature  or  setting 
free  the  lactic  acid.  It  must  be  remembered  that  to 
obtain  curative  results  by  this  method  it  is  necessary 
to  repeat  the  process  daily  perhaps  for  a  number  of 
weeks,  and,  if  we  over-stimulate  the  skin  by  heat,  we 
shall  exhaust  the  patient  and  also  depress  the  activity 
of  the  skin.  Some  of  the  most  difficult  cases  I  have 
met  with  as  regards  restoring  the  functions  of  the  skin 
have  been  patients  who  have  had  prolonged  courses  of 
Turkish  baths,  using  the  hottest  room,  or  patients  who 
had  lived  for  many  years  in  hot  dry  climates.  It  must 
be  remembered  that  Turkish  baths  originated,  and  are 
most  used,  in  hot  climates  where  the  skin  acts  too 
copiously,  and  the  desired  effect  of  these  baths  is  to 
limit  the  overaction  of  the  skin. 

For  purposes  of  treatment  we  need  the  lowest  tem- 
perature which  will  accomplish  the  result,  and  applied 
through  a  vehicle  which  will  check  heat  radiation  from 
\  the  skin. 

In  experiments,  made  many  years  ago,  I  found  that 
I  could  obtain  the  maximum  rise  of  body  tempera- 
ture with  the  minimum  of  heat  by  using  moist  warm 
air  at  103°  to  105°  F.  This  was  in  patients  whose 
temperature  was  subnormal  or  who  had  inactive  skins. 
When  the  temperature  is  above  normal,  or  the  skin  is 
active,  a  lower  temperature  is  desirable,  because,  if 
we  produce  free  action  of  the  skin  too  quickly,  the 
temperature  does  not  rise  to  the  same  degree.  We 
diminish  the  rise  in  the  body  temperature  by  increasing 
the  external  heat  employed.  This  is  a  fact  which  the 
uneducated  find  it  difficult  to  understand. 

The  ordinary  immersion  bath  will  raise  the  body 
temperature,  but  water  in  contact  with  the  skin  checks 
cutaneous  excretion,  and,  unless  this  occurs  after  the 


PYRETIC    TREATMENT  121 

patient  leaves  the  bath,  is  apt  to  cause  the  feelings  of 
congestion  I  have  described. 

Hot  baths  do  not  greatly  influence  the  excretion  of 
lactic  acid.  We  have  evidence  of  this  in  the  fact  that 
they  do  not  remove  from  the  skin  the  dead  epithelial 
cells,  which  requires  lactic  acid  to  overcome  their 
cohesion  to  the  living  cells,  as  I  have  explained  in  a 
previous  chapter. 

Steam  and  vapour  baths  raise  the  body  temperature, 
and  the  cutaneous  action  is  only  to  a  small  degree 
checked  by  the  condensation  of  the  vapour  on  the  skin. 
It  is  not  an  ideal  method,  but  efficient  enough  in  many 
cases  if  it  can  be  used  with  the  patient  in  the  horizontal 
position.  As  steam  baths  dilate  the  blood-vessels,  the 
sitting  position  is  undesirable.  The  crudest  form  of 
bath  I  have  seen  is  an  electric  bath  in  which  the  patient 
sits  on  a  stool  with  his  head  through  a  hole  in  a  box, 
surrounded  by  electric  lights  which  give  a  perfectly 
dry  heat.  This  is  the  antithesis  of  pyretic  treatment. 

In  my  own  practice,  where  forty  or  fifty  treatments 
have  to  be  given  daily,  it  is  necessary  to  have  some 
convenient  appliance  which  enables  the  maximum 
efficiency  to  be  attained  with  the  minimum  of  labour. 
Many  years  ago,  I  designed  a  '  thermal  couch'  which 
has  met  every  requirement.  It  consists  of  an  iron 
bedstead,  the  mattress  of  which  is  a  double  layer  of 
fine-mesh  galvanized  netting.  On  this  are  placed  six 
blankets  and  a  bath  sheet.  The  patient  lies  upon  these, 
with  a  pillow,  as  if  in  bed.  A  hinged  metal  cover  is 
placed  over  him,  covering  the  feet  and  reaching  to  the 
shoulders  ;  the  opening  here  is  closed  by  a  blanket,  so 
that  only  the  head  is  left  uncovered.  Beneath  the 
wire  mattress  is  a  copper  receptacle  covering  the  whole 
bed,  and  closed  at  the  bottom  and  sides.  The  sides 


122  PYRETIC    TREATMENT 

slope  to  the  centre  to  allow  the  water  of  condensation 
to  run  away  to  a  small  pipe  which  acts  as  a  drain. 
Into  this  chamber  steam  is  ejected  from  a  self-filling 
boiler.  The  steam  heats  the  blankets  upon  which  the 
patient  lies,  and  finding  its  way  through  them,  deposits 
all  superfluous  moisture,  and  fills  the  chamber  in  which 
the  patient  lies  with  warm  moist  air.  This  appliance 
produces  a  rise  of  temperature  of  3°  to  4°  F. 

The  apparatus  which  I  described  in  1893,  and  had 
used  for  five  years  previously,  was  intended  for  the 
treatment  of  acute  rheumatism  or  any  condition  where 
it  was  necessary  to  apply  the  process  without  removing 
the  patient  from  his  own  bed.  It  consists  essentially 
of  a  double-metal  cover,  which  can  be  placed  over 
the  patient  from  the  feet,  where  it  is  closed,  to  the 
shoulders.  Between  the  two  pieces  of  metal  is  a 
quarter-of-an-inch  space  which  is  filled  with  boiling 
water  immediately  before  it  is  used.  The  patient  lies 
upon  a  blanket,  a  hot  moist  blanket  is  placed  over  the 
front  of  the  body,  and  then  the  cover  is  placed  over 
the  patient.  For  convenience,  it  is  divided  into  two 
parts,  one  for  the  lower  extremities  and  the  other  for 
the  trunk.  The  result  is  that  the  patient  is  surrounded 
with  warm  moist  air. 

The  effect  of  this  appliance  is  to  cause  a  rise  of 
temperature  of  2°  to  3°  F.  Sweating  usually  commences 
in  fifteen  to  twenty-five  minutes  according  to  the  con- 
dition of  the  patient.  When  sweat  appears  on  the  fore- 
head of  the  patient,  it  is  the  signal  to  finish  the  process. 
It  does  not  increase  the  efficiency  to  continue  it  longer, 
and  if  sweating  occurs  too  quickly  it  is  a  sign  that  the 
temperature  used  has  been  too  high. 

A  large  number  of  patients  who  require  treatment 
have  chronic  valvular  disease  of  the  heart.  The  effect 


PYRETIC    TREATMENT  123 

is  to  stimulate  the  heart  and  improve  the  tone  of  the 
pulse.  In  the  many  thousands  of  treatments  given 
during  the  last  twenty-five  years  we  have  never  had  a 
case  where  the  slightest  untoward  symptom  has  occured 
while  the  patient  was  on  the  thermal  couch.  Many 
patients  over  eighty  years  of  age  take  daily  treatment 
for  a  long  period,  and  are  not  exhausted  either  at  the 
time  or  subsequently,  because  fever,  of  short  duration, 
is  a  most  powerful  physiological  tonic.  It  is  not 
unusual  for  patients  taking  the  treatment  for  the  first 
few  times  to  have  a  feeling  of  oppression  before  the 
cutaneous  excretion  commences  ;  but  it  is  common  to 
all  baths  which  raise  the  body  temperature,  for  the 
reason  I  have  explained. 

Immediately  after  the  treatment  the  patient  is 
usually  given  a  spray  or  needle-bath,  in  order  to  restore 
the  tone  of  the  cutaneous  blood-vessels.  It  happens 
rarely  that  patients  may  feel  faint  during  this  process, 
and  it  may  be  necessary,  especially  in  cases  of  dilated 
heart,  to  substitute  tepid  sponging  ;  but  of  course  the 
great  majority  regard  the  needle-bath  as  the  most 
enjoyable  part  of  the  process.  A  large  number  of 
patients  go  out  of  doors  in  all  wreathers  soon  after  the 
treatment,  but  I  have  never  yet  traced  a  chill  or  a  cold 
to  this  cause.  The  greater  physiological  activity  of 
the  skin  has  the  effect  of  increasing  resistance  to 
atmospheric  conditions. 

Every  patient  has  the  night  and  morning  temperature 
taken,  and  if  the  morning  temperature  begins  to  fall, 
it  is  an  indication  that  the  treatment  is  over-stimu- 
lating. Such  cases  are  of  rare  occurrence,  but  I  think 
all  treatment  of  this  kind  should  be  accompanied  by. 
exact  observations. 

Usually  patients  feel  distinctly  better  directly  after 


124  PYRETIC     TREATMENT 

and  during  the  course  of  treatment,  long  before  the 
joint  symptoms  show  signs  of  improvement ;  but  it 
may  happen  that  a  patient  feels  a  certain  amount  of 
malaise  during  the  course  or  at  some  part  of  it. 
Usually  in  these  cases  there  is  a  continued  rise  of  tem- 
perature, produced  by  the  process.  It  is  so  slight 
that  the  patient  is  not  aware  of  it  ;  but  when  it 
happens  it  greatly  shortens  the  necessary  duration  of 
treatment. 

A  large  proportion  of  patients  have  a  subnormal 
temperature.  If  it  rises  to  normal  and  continues  at, 
or  a  little  above,  the  normal  line,  it  represents  a  true 
fever,  and  it  will  fall  to  the  normal  of  the  patient 
directly  the  'fever'  abates.  We  thus  frequently 
produce  attacks  of  'rheumatic  fever'  which  are  only 
recognizable  on  the  temperature  chart. 

Some  patients  who  may  appear  in  good  health  will 
complain  of  feeling  exhausted  after  the  bath,  for  no 
very  obvious  reason.  In  these  patients  there  is  almost 
always  a  spinal  irritability,  and  the  heat  over-stimulates 
the  nerve  centres  and  produces  exhaustion.  A  folded 
towel  placed  down  the  spine,  by  protecting  it  from 
heat,  will  prevent  this  trouble. 

Whether  we  watch  the  effect  of  natural  fever  in 
eliminating  lactic  acid  from  the  tissues,  or  the  effect 
of  pyretic  treatment,  we  have  to  recognize  that  the 
process  is  a  slow  one.  Most  often  in  rheumatic  fever 
the  temperature  falls  and  the  joint  symptoms  disappear 
before  all  the  acid  is  removed  from  the  tissues,  and 
unless  we  take  steps  to  prolong  the  fever  we  are  sure  of 
subsequent  trouble.  In  pyretic  treatment  we  are  not 
concerned  with  the  improvement  of  the  joints  as  an 
indication  that  we  have  attained  our  results.  The  real 
clinical  indication  is  the  reaction  of  the  skin  :  until 


PYRETIC    TREATMENT  125 

it  resumes  the  normal  very  slightly  acid  or  neutral 
reaction,  the  patient  is  not  cured. 

On  this  point  there  is  marked  difference  between  the 
lactic-acid  patient  and  the  one  with  a  lithic  diathesis. 
The  lactic-acid  patient  starts  with  a  very  acid  reaction, 
and  this  will  continue  very  slowly  diminishing  until 
the  normal  is  attained.  The  lithic  or  'gouty'  patient 
will  start  with  a  neutral  or  slightly  acid  reaction,  and 
this  will  become  slowly  more  acid  until  a  point  is  reached 
when  the  whole  body  may  give  a  very  acid  reaction, 
and  then  it  will  gradually  decrease  in  acidity  until  it 
is  neutral  or  very  slightly  acid.  When  this  point  is 
reached  we  cannot  say  that  the  patient  is  free  from 
lithates  ;  it  only  means  that  we  have  set  free  all  the 
available  lactic  acid,  and  this  has,  so  far  as  it  has 
been  able,  dissolved  up  these  lithates. 

If  we  continued  the  treatment  under  these  conditions 
we  should  not  make  any  further  improvement.  If  the 
patient  now  takes  active  exercise,  taking  due  care  to 
maintain  the  skin  in  action,  he  will  go  on  improving, 
and  if  at  the  end  of  six  months  he  has  another  course 
of  treatment,  marked  improvement  will  result.  For 
this  reason,  while  in  rheumatism  the  best  effects  are 
obtained  from  a  long  course  of  treatment,  for  gout  two 
shorter  courses  will  generally  yield  better  results,  and 
may  be  regarded  as  necessary  in  most  cases. 

The  value  of  pyretic  treatment  will  never  be  fully 
recognized  until  it  becomes  employed  by  the  prac- 
titioner in  suitable  cases.  When  this  happens,  we  shall 
no  longer  have  the  patients  with  easily  curable  forms 
of  rheumatism  allowed  to  drift  on  until  they  become 
helpless  cripples  and  a  burden  on  society.  This  is 
not  a  theoretical  statement,  but  the  result  of  thirty 
years'  daily  experience.  It  is  less  easy  to  carry  out 


126  PYRETIC     TREATMENT 

pyretic  treatment  than  it  is  to  write  a  prescription  ; 
but  there  are  few  households  where  all  that  is  neces- 
sary for  early  treatment  does  not  exist,  and  the  only 
thing  needful  is  the  assistance  of  some  person  fitted  to 
carry  out  the  details  of  the  treatment. 

The  hot  moist  blanket  pack  is  an  efficient  form  of 
pyretic  treatment  in  many  cases.  The  requirements  are 
four  blankets  laid  upon  a  bed,  and  a  thinner  blanket, 
well  wrung  out  of  hot  water,  placed  on  the  top  of  these. 
The  patient  lies  in  the  centre  of  the  moist  blanket, 
which  is  drawn  round  him,  and  then  each  of  the  dry 
blankets  is  in  turn  folded  over  the  patient,  tucked  well 
in  at  the  sides  and  round  the  shoulders.  A  hot- water 
bottle  to  the  feet,  and  a  down  quilt  to  cover  all,  are  of 
advantage.  The  only  difficulty  in  this  process  is  the 
moist  hot  blanket.  It  is  best  prepared  by  folding  it, 
rolling  it  up  like  a  rug  used  for  travelling,  and  then 
placing  it  on  end  in  a  bucket.  Boiling  water  is  now 
poured  through  the  centre  to  moisten  it  completely. 
It  is  then  thrown  into  a  large  towel,  and  can  best  be 
deprived  of  all  superfluous  moisture,  which  is  necessary, 
by  two  people  twisting  the  towel  at  either  end.  It  is 
this  part  of  the  process  which  may  be  difficult  in  some 
cases,  when  the  necessary  service  cannot  be  obtained. 
The  hot  blanket  pack  can  be  improved  upon,  and  a 
greater  rise  of  temperature  attained,  by  interposing  a 
mackintosh  sheet  or  an  oil  sheet  between  the  first  and 
second  dry  blankets.  This  prevents  evaporation,  and 
more  efficiently  prevents  the  radiation  of  heat  from  the 
body. 

A  simple  method,  well  adapted  for  domestic  use, 
without  skilled  help,  is  the  '  foot-bath  pack '.  Four 
blankets  are  spread  on  a  comfortable  arm-chair,  in  such 
a  way  that  they  have  six  inches  of  their  lower  borders 


PYRETIC    TREATMENT  127 

on  the  ground.  A  foot-bath  is  half  filled  with  hot  water 
and  placed  in  front  of  the  chair.  The  patient,  clad  in 
flannel  pyjamas  or  nightgown,  sits  on  the  chair  and 
puts  his  feet  into  the  hot  water.  The  blankets  are  now 
folded  over  the  bath  and  the  patient,  so  as  to  prevent 
the  escape  of  steam,  and  also  so  that  no  cold  air  is 
admitted.  Care  on  this  point  is  the  essential  factor 
in  producing  the  result.  In  about  ten  minutes,  more 
hot  water  is  added  to  the  foot-bath  by  opening  the 
blankets  just  sufficiently  to  do  so,  and  this  may  be 
repeated  if  required.  In  twenty-five  to  thirty  minutes 
the  temperature  of  the  patient  is  usually  raised  about 
2°  F.,  and  there  is  a  good  perspiration.  The  patient 
then  gets  into  a  blanket-bed,  the  feet  only  being  quickly 
rather  than  completely  dried.  This  is  a  very  useful 
treatment  when  a  patient  in  good  health  has  been 
exposed  to  a  chill,  or  for  elderly  or  feeble  invalids  who 
require  treatment  with  the  minimum  of  fatigue.  It  is 
not  efficient  in  cases  where  there  has  been  prolonged 
functional  inactivity  of  the  skin,  such  as  we  find  in  the 
lithic  diathesis,  but  it  may  be  used  to  maintain  functional 
activity  when  this  has  been  secured  by  other  means. 

Although  it  is  a  simple  method,  its  success,  like  all 
balneological  methods,  depends  upon  attention  to 
detail  and  a  clear  understanding  of  the  principles 
involved.  The  hot  water  raises  the  temperature  of  the 
blood  as  it  circulates  through  the  feet.  The  blankets, 
being  wrapped  closely  around  the  patient,  check  the 
radiation  of  this  heat.  Therefore  the  higher  the 
temperature  of  the  water,  and  the  more  efficiently  the 
packing  is  performed,  the  greater  will  be  the  rise  of  the 
body  temperature. 

In  many  cases  of  a  chronic  character  the  ordinary 
vapour  baths  give  good  results.  The  portable  vapour 


128  PYRETIC     TREATMENT 

baths  sold  for  this  purpose  have  the  disadvantage  that 
the  steam  enters  the  cabinet  too  high  above  the  floor, 
so  that  the  feet  remain  cold.  It  is  always  advisable  to 
have  the  patient's  feet  in  a  foot-bath,  to  which  a  little 
washing-soda  may  be  added  with  advantage.  In 
chronic  rheumatism,  if  the  smell  is  not  objected  to, 
a  solution  made  by  boiling  sulphur  with  washing-soda, 
added  to  the  foot-bath,  is  helpful. 

One  cannot  attain  the  efficiency  of  more  elaborate 
apparatus  by  these  simple  methods,  but  they  are  capable 
of  doing  an  enormous  amount  of  good  if  they  are  carried 
out  persistently,  if  the  practitioner  is  not  deterred 
by  some  aggravation  of  the  symptoms  in  certain  cases, 
and,  beyond  all,  if  he  does  not  expect  the  acid  which 
may  have  taken  years  to  accumulate  to  be  removed  in 
a  week  or  two  of  treatment.  I  remember  one  case  in 
my  early  experience.  A  physician  who  adopted  my 
views  with  great  enthusiasm,  and  whom  I  had  supplied 
with  special  apparatus,  wrote  me  to  say  that  he  had 
given  a  military  man  with  chronic  rheumatic  gout 
twenty  of  my  baths  and  he  was  still  uncured  ;  there- 
fore, as  he  did  not  know  what  to  do,  he  sent  him  to 
see  me.  I  simply  gave  him  twenty  more  baths,  and 
he  made  such  a  good  recovery  that  he  was  permitted 
to  re-enter  the  Army  during  the  Boer  War,  and  subse- 
quently became  a  distinguished  general. 

Another  cause  of  failure  is  to  mistake  great  improve- 
ment in  the  joint  symptoms  for  a  cure  of  the  condition. 
The  only  reliable  test  is  the  reaction  of  the  skin.  I 
have  already  pointed  this  out,  but  it  is  of  enormous 
importance.  I  am  less  concerned  with  the  condition 
of  a  patient  immediately  after  treatment  than  I  am 
with  his  condition  six  months,  or  several  years,  later. 
It  is  the  life-history  of  patients  from  which  we  learn 


PYRETIC    TREATMENT  129 

most  in  these  cases.  Thus  a  gentleman  82  years  of 
age  was  very  much  crippled  by  rheumatic  gout.  After 
a  month's  treatment  he  was  decidedly  better,  but  still 
very  infirm.  Nine  years  later  he  came  to  me  with 
pain  in  the  muscles  of  the  thighs,  which  I  found  to  be 
due  to  his  practice  of  walking  over  a  very  steep  hill 
every  morning  as  a  constitutional.  There  was  no 
trace  of  the  original  joint  trouble,  and  at  the  age  of  91 
he  was  taking  long  walks  every  day  which  would  have 
fatigued  most  men  of  middle  age. 

There  is  another  form  of  pyretic  treatment  very 
valuable  in  certain  cases  :  it  simply  consists  in  active 
exercise  of  any  kind  when  the  body  is  over-clothed 
with  wool  next  the  skin.  Free  action  of  the  skin  is 
produced  and  the  temperature  rises.  The  patient  then 
removes  the  garments  and  sponges  the  body  with  hot 
water  before  resuming  his  ordinary  garments.  The 
treatment  is  only  adapted  to  fairly  robust  patients  and 
those  of  the  lithic  diathesis.  It  is  not  advisable  for 
those  of  the  lactic-acid  diathesis,  as,  while  it  aids  the 
elimination  of  lactic  acid,  it  also  increases  its  production. 
It  is  probably  because  muscular  exercise  increases  the 
production  of  lactic  acid  that  those  who  have  accumu- 
lated too  much  are  prevented  from  making  more  by 
the  stiffening  of  their  organs  of  locomotion.  Nature  is 
wonderfully  protective  in  her  methods,  and  uses  lactic 
acid  to  prevent  us  from  over-working  our  muscles 
even  in  health. 

There  is  another  method  of  pyretic  treatment  so 
simple  that  it  hardly  appears  necessary  to  mention  it, 
but  which  is  of  great  value  in  overcoming  the  immediate 
effects  of  a  chill.  It  is  simply  for  the  patient  to  lie  on 
a  blanket  at  night  and  have  an  extra  amount  of  bed- 
clothes to  cover  him.  This  will  often  induce  a  reaction 

9 


130  PYRETIC     TREATMENT 

accompanied  by  free  action  of  the  skin,  and  a  great 
deal  of  future  trouble  may  be  averted. 

The  administration  of  vaccines  may  be  regarded  as  a 
form  of  pyretic  treatment  when  a  decided  '  reaction ' 
is  induced.  Until  proof  can  be  given  to  the  contrary, 
I  am  inclined  to  attribute  any  good  results  attained  to 
the  fever  produced,  rather  than  to  the  nature  of  the 
vaccine  which  caused  the  reaction. 

Treatment  by  mineral  baths  is  another  form  of  pyretic 
treatment.  The  constituents  of  the  mineral  waters 
may  vary  ;  but  most  of  them  have  a  certain  reputation 
in  the  treatment  of  gout  and  rheumatism,  and  all  have 
a  common  effect  in  producing  a  certain  amount  of 
pyrexia  during  the  bath. 

It  is  usual  at  such  spas  to  give  a  bath  on  alternate 
days,  clinical  experience  showing  that  more  frequent 
baths  may  exhaust  the  patient.  Such  clinical  experi- 
ence is  entirely  founded  upon  failure  to  administer  baths 
on  physiological  principles.  The  temperature  of  the 
body  may  be  raised,  and  lactic  acid  set  free,  without 
its  excretion  by  the  skin.  This  produces  the  feeling  of 
malaise  I  have  described.  Or  there  may  be  free  action 
of  the  skin  and  dilatation  of  the  blood-vessels,  and  no 
means  subsequently  taken  to  ensure  their  contraction. 
In  these  circumstances  the  bath  is  relaxing.  If  baths 
are  properly  given  there  are  very  few  patients,  if  any, 
who  cannot  take  one  daily  with  advantage.  The 
importance  of  this  is  that  the  period  during  which 
patients  remain  for  treatment  is  limited.  Four  weeks 
is  regarded  as  a  long  visit,  and  if  at  the  end  of  that 
time  they  have  only  taken  a  dozen  baths,  only  a  limited 
amount  of  lactic  acid  will  have  been  eliminated,  and 
the  results  are  by  no  means  as  satisfactory  as  they 
might  have  been. 


PYRETIC    TREATMENT  131 

It  is  only  when  daily  observations  are  taken  of  the 
reaction  of  the  skin  that  we  know  anything  of  the 
results  of  baths,  and  when  we  do  this  we  learn  that 
acids  which  have  been  accumulating  in  the  tissues  for 
years  are  not  removed  by  a  dozen  baths.  In  the  lithic 
diathesis  it  frequently  requires  twelve  baths  to  bring 
the  patient's  skin  to  its  maximum  of  acidity,  and  if 
the  baths  are  discontinued  at  this  stage  the  patient  is 
more  liable  to  an  attack  of  acute  lithitis  than  before 
treatment. 

Thirty  years'  daily  observation  of  the  effects '  of 
pyretic  treatment  of  all  kinds  has  greatly  impressed  me 
with  the  fact  that  cases  of  chronic  gout,  rheumatism, 
and  arthritis,  in  which  a  hopeless  prognosis  has  been 
given,  are  perfectly  curable  ;  but  it  has  also  taught  me 
that  these  results  can  only  be  attained  by  prolonged 
and  systematic  treatment  adapted  to  the  patients' 
physiological  requirements,  and  as  to  this  we  can  only 
be  guided  by  exact  observations.  The  mineral  spas  of 
Europe  have  done  great  good  in  many  cases,  but  the 
results  within  their  capacity  have  never  been  attained, 
because  their  routine  methods  have  no  scientific  basis. 


132 


CHAPTER    X. 

GOUT  AND   THE   LITHIC    DIATHESIS. 

WE  find  lithates  around  the  joints  in  persons  who  are 
in  a  state  of  good  physical  health,  and  such  persons 
may  never  have  an  attack  of  gout.  But,  as  I  have 
pointed  out,  those  who  have  a  tendency  to  the  forma- 
tion of  lithates  have  usually  a  subnormal  temperature, 
and  the  skin  may  be  more  or  less  inactive.  Although 
this  is  the  case,  it  does  not  follow  that  complete  inactivity 
of  the  skin  is  of  necessity  followed  by  the  formation  of 
lithates,  or  that  a  skin  capable  of  performing  its  function 
is  incompatible  with  their  production. 

When  we  shake  hands  with  a  person  of  the  lithic 
diathesis  we  find  the  skin  dry  and  smooth  to  the  touch, 
and  the  muscles  convey  a  sense  of  resiliency.  When 
we  shake  hands  with  a  patient  having  true  '  rheumatoid 
arthritis'  there  is  a  marked  loss  of  muscular  resiliency. 
The  contrast  between  the  handshake  of  such  patients 
and  those  of  the  lithic  diathesis  is  so  marked,  that  it  is 
quite  sufficient  to  distinguish  between  the  two  cases 
without  any  further  examination.  At  a  time  when 
patients  of  the  gouty  and  rheumatic  class  are  commonly 
diagnosed  as  having  'rheumatoid  arthritis',  this  ready 
means  of  distinction  is  very  important. 

We  are  so  accustomed  to  be  told  that  gout  is  due  to 
an  excess  of  acid  in  the  blood  that  it  may  at  first  be 
difficult  to  appreciate  the  fact  that  one  of  the  great 
factors  in  the  formation  of  the  lithates  is  the  absence 
of  free  lactic  acid  in  the  lymph-space.  This  apparent 


GOUT    AND    THE    LITHIC    DIATHESIS      133 

contradiction  is  due  to  the  fact  that  the  conditions  caus- 
ing the  formation  of  the  insoluble  lithates  are  not  the 
same  as  those  which  produce  the  attack  of  gout.  The 
confusion  of  thought  which  exists  is  due  to  the  fact  that 
two  separate  physiological  processes  have  always  been 
considered  as  due  to  the  same  factors.  Not  only  is 
this  not  the  case,  but  also  the  formation  of  lithates  in 
the  tissues  is  not  of  necessity  followed  by  the  symptoms 
we  recognize  as  gout.  This  point  can  be  easily  demon- 
strated under  certain  conditions. 

A  lady  whose  skin  had  been  in  a  state  of  entire 
inactivity  since  infancy,  and  had  become  hard  and  dry 
from  the  accumulation  of  epithelial  cells,  and  who  had 
occasional  attacks  of  dry  eczema  on  the  hands  and  face 
from  the  effects  of  exposure  to  air,  was  otherwise  very 
robust  and  took  a  large  amount  of  active  exercise. 
An  examination  of  the  joints  showed  an  entire  absence 
of  lithates.  But  if  this  patient  was  confined  to  her 
bed  for  a  week  from  any  cause,  lithates  appeared  in  all 
the  large  joints  and  gave  audible  evidence  of  their 
existence.  Directly  she  resumed  active  exercise  they 
at  once  disappeared,  and  she  at  no  time  had  any  sym- 
ptoms of  gout  or  swelling  and  pain  in  her  joints. 

It  is  obvious  in  this  case  that  rest  caused  diminution 
in  the  flow  of  lymph  to  the  tissues,  and  also  of  lactic 
acid,  the  natural  solvents  of  the  phosphate  of  lime  in 
the  dead  cells,  and  the  result  was  that  the  salt  was 
partially  oxidized  and  became  less  soluble.  Directly 
exercise  was  resumed,  sufficient  lymph  and  lactic  acid 
was  supplied  to  dissolve  those  concretions  which  had 
not  become  stable,  and  they  disappeared. 

\Yhile  the  skin  is  more  or  less  inactive  in  the  lithic 
diathesis,  the  diminution  of  its  excretory  power  is  not 
a  direct  cause  of  the  deposit  of  lithates,  but  because 


134     GOUT    AND    THE    LITHIC    DIATHESIS 

the  physiological  inactivity  of  the  skin  is  accompanied 
by  diminution  of  lymph  in  the  lymph-space.  The 
result  is  that  we  have  two  classes  of  lithic  patients^  so 
far  as  their  joint  conditions  are  concerned. 

The  patient  whose  skin  may  be  normally  active,  but 
who  never  takes  any  exercise  to  excite  its  activity, 
will  accumulate  a  large  amount  of  lithates  in  the  joints, 
and  this  accumulation  may  not  of  necessity  be  accom- 
panied by  any  active  joint  trouble.  By  the  process  of 
oxidation  the  lactophosphate  of  lime  becomes  more 
and  more  insoluble,  and  the  concretions  take  the 
form  more  of  plaster-of-Paris  than  of  chalk,  because 
it  is  harder  and  drier.  This  is  the  feeling  it  con- 
veys when  the  joint  is  put  through  its  movements. 
The  crepitations  are  frequently  audible,  although  the 
examination  may  be  painless.  But  when  subacute 
inflammatory  symptoms  appear  in  one  of  these  joints, 
the  crepitations  in  this  joint  at  once  become  softer, 
showing  that  the  deposit  is  receiving  a  larger  amount 
of  moisture. 

We  have  another  class  of  lithic  patient  whose  life 
may  be  sedentary  but  who  regularly  takes  vigorous 
exercise.  He  may  play  golf  or  tennis.  During  such 
exercise  his  skin  may  act  freely,  but  there  is  no  tendency 
to  do  so  in  the  intervals.  We  may  find  his  temperature 
subnormal,  and  that  he  is  rather  sensitive  to  cold,  but 
is  otherwise  quite  robust.  This  man,  during  the 
sedentary  periods  of  life,  will  form  lithates  in  the  tissues 
which  are  redissolved  during  active  exercise.  The 
result  is  that  the  act  of  exertion  causes  a  large  amount 
of  soluble  lactophosphate  of  lime  to  appear  in  the 
lymphspace ;  and  even  if  free  action  of  the  skin  allows 
some  of  it  to  be  excreted,  it  does  not  continue  long 
enough  to  get  rid  of  the  whole,  and  this  has  to  find 


GOUT    AND    THE    LITHIC    DIATHESIS     135 

its  way  by  the  lymphatics  to  the  thoracic  duct  and 
hence  to  the  kidneys,  where  it  is  excreted. 

In  these  cases  we  do  not,  as  a  rule,  find  much 
deposit  of  lithates  in  the  joints.  If  we  do  find  them, 
it  is  usually  in  some  tissue  which  at  one  time  or  another 
has  been  sprained  through  an  accident  and  a  certain 
degree  of  physiological  inactivity  has  resulted,  or  we 
may  find  it  in  the  great-toe-joint,  or  shoulder.  If  the 
lactophosphate  of  lime  passes  through  the  kidney  in 
a  soluble  form,  it  gives  no  visible  sign  of  its  presence  ; 
but  as  I  have  explained  in  the  chapter  on  uric  acid,  it 
may  set  up  those  chemical  transformations  which  result 
in  the  excretion  of  lithates  or  uric  acid  in  its  insoluble 
form.  This  result  is  so  common  when  a  man  of  seden- 
tary life  takes  active  exercise  that  we  rather  expect  it. 
It  is  only  when  it  frequently  occurs,  and  especially  when 
not  only  uric  acid  is  formed  but  also  small  concretions, 
that  we  regard  it  as  a  symptom  of  the  '  gouty '  diathesis. 
The  continuance  of  this  condition,  even  when  the  lacto- 
phosphate of  lime  in  excess  is  passed  in  its  soluble  form,, 
has  a  very  injurious  effect  upon  the  kidney. 

I  am  not  in  a  position  to  state  what  exactly  happens. 
The  kidney  may  not  show  by  ordinary  tests  any  impair- 
ment of  its  functions ;  but  when  we  test  it  for  its  capacity 
to  excrete  lactophosphate  of  lime,  we  find  it  is  very 
deficient.  This  can  easily  be  done  by  saturating  a 
specimen  of  the  urine  with  chloride  of  ammonium  and 
then  adding  liquor  ammonise  fortis  and  noticing  the 
amount  of  precipitate  which  falls  when  the  urine  has 
been  allowed  to  stand  for  a  little  while. 

It  is  not  uncommon,  in  cases  with  no  symptoms 
which  would  usually  be  attributed  to  gout,  to  find  that 
the  kidney  is  excreting  no  lactophosphate  of  lime,  or 
only  a  very  small  quantity.  In  these  cases  the  urine 


136     GOUT    AND    THE    LITHIC    DIATHESIS 

is  usually  very  acid,  and  there  may  be  some  irritation 
of  the  bladder ;  but,  as  I  have  previously  stated,  a 
symptom  which  sometimes  calls  attention  to  the  failure 
is  attacks  of  giddiness  which  may  come  on  when  the 
patient  is  at  rest,  and  be  worse  when  moving  about. 
In  the  absence  of  other  causes  for  this  trouble  it  is 
always  well  to  test  the  urine  in  the  way  I  have  suggested. 
Such  cases  point  very  clearly  to  the  absolute  necessity 
of  restoring  and  maintaining  the  activity  of  the 
cutaneous  excretion  in  patients  of  the  lithic  type. 
Although  the  kidneys  may  for  many  years  perform 
the  functions  for  which  the  skin  is  intended,  the  work 
thrown  upon  them  will  sooner  or  later  impair  their 
functional  activity  for  this  particular  work,  and  as  a 
natural  result  we  have  those  cases  where  there  is  an 
accumulation  of  lactophosphate  of  lime  in  the  blood 
and  the  lymph  which  we  associate  with  uric  acid,  and 
all  the  symptoms  which  follow  from  it. 

Between  the  two  classes  of  lithic  patients  I  have 
described,  there  are  a  great  variety  of  gradations 
according  to  the  life  led  by  the  patients  and  the  condi- 
tions to  which  they  are  exposed. 

Another  characteristic  symptom  which  we  notice  in 
patients  of  the  lithic  diathesis  is  the  tendency  for  the 
hair  to-  turn  grey  or  white,  prematurely.  This  sym- 
ptom occurs  in  persons  whose  health  and  general 
constitution  is  perfectly  sound.  It  is  not  due  to  the 
excretion  of  lactic  acid,  because  examination  of  the 
scalp  of  such  patients  gives  usually  a  neutral  reaction, 
except  during  the  act  of  sweating.  I  found  in  many 
cases  that  the  reaction  of  the  dry  scalp  tended  to 
decolorize  moistened  litmus  paper.  This  led  me  to 
suspect  lactate  of  ammonia,  and  consequently  I  made 
a  point  of  examining  the  cutaneous  excretion  of  the 


GOUT    AND    THE    LITHIC    DIATHESIS      137 

scalp,  during  the  act  of  sweating,  for  ammonia.  I  have 
found  it  so  frequently  in  such  cases  that  I  can  say, 
with  confidence,  that  the  cause  of  the  prematurely 
grey  hair  in  such  cases  is  the  excretion  of  lactate  of 
ammonia.  The  fact  that  patients  with  the  lithic 
diathesis  form  a  large  amount  of  lactate  of  ammonia — 
and  we  find  it  with  great  frequency  in  the  cutaneous 
excretion  of  the  whole  body — may  partially  explain  their 
incapacity  to  dissolve  the  lithates  in  the  tissues.  It 
may  not  be,  always,  the  absence  of  lactic  acid,  but  the 
fact  that  when  it  is  set  free  it  becomes  locked  up  as 
lactate  of  ammonia,  and  this  would  have  no  solvent 
action  upon  phosphate  of  lime. 

The  effect  of  cold,  by  limiting  the  amount  of  fluid 
in  the  lymph-space,  is  an  important  factor  in  causing 
the  formation  of  lithates.  Formerly  gout  was  regarded 
as  a  disease  almost  peculiar  to  men  ;  at  the  present 
time,  in  certain  forms,  it  is  more  common  amongst 
women,  the  reason  being  that  the  majority  of  women 
have  a  great  objection  to  clothing  themselves  warmly. 
They  appear  to  suffer  less  discomfort  than  men  from 
the  effects  of  cold,  but  the  physiological  effect  is  the 
same.  The  woman  whose  hands  are  always  cold  will 
at  a  later  period  show  lithates  around  the  joints,  and 
especially  if  she  does  not  take  much  active  exercise. 
The  condition  most  favourable  to  the  formation  of 
lithates  is  for  a  person  to  sit  in  a  cold  room  until  the 
surface  of  the  body  is  chilled.  The  lack  of  lactic  acid, 
owing  to  the  inactivity  of  the  muscles  and  the  absence 
of  fluid  in  the  lymph-space,  renders  it  impossible  for  the 
normal  process  of  metabolism  to  be  carried  on. 

There  are  two  important  facts  to  be  remembered  in 
respect  of  this.  Rheumatism  and  gout  are  more 
prevalent  in  Great  Britain  than  in  any  other  country. 


138      GOUT    AND    THE    LITHIC    DIATHESIS 

The  houses  in  Great  Britain  are  worse  heated  than  any 
in  the  civilized  world.  It  might  be  thought  that 
Canadians,  inured  as  they  are  to  excessive  cold  in 
winter,  would  find  the  climate  of  this  country  much 
more  acceptable.  On  the  contrary,  they  complain  of 
the  great  coldness  of  the  British  house,  and  suffer  from 
it.  This  question  is  so  important  in  connection  with 
the  prevention  of  gout  and  rheumatism  that  I  do  not 
consider  it  a  digression  to  consider  it. 

In  this  country  our  domestic  heating  depends  mostly 
upon  coal  fires  and  gas  stoves.  Both  of  these  give 
radiant  heat  which  warms  the  objects  in  the  room  but 
not  the  air  which  surrounds  them.  As  a  result  we  may 
burn  our  knees  by  sitting  too  close  to  the  fire,  while 
the  surface  of  the  back  is  chilled.  Incidentally,  the 
methods  used  to  produce  radiant  heat  allow  60  per 
cent  of  the  heat  to  escape  up  the  chimney  in  the  flue- 
pipe. 

On  the  Continent  and  in  the  Colonies  domestic  heat- 
ing is  attained  more  generally  by  the  use  of  stoves  and 
central  heating.  This  gives  convected  heat  which 
raises  the  temperature  of  the  air  of  the  room.  If  too 
high  a  temperature  is  produced  and  there  is  an  absence 
of  ventilation,  this  method  is  objectionable ;  but  to 
use  such  methods,  so  as  to  secure  a  temperature  of 
60°  to  65°  in  the  room,  and  at  the  same  time  use  the 
source  of  heat  as  a  means  of  ventilation,  is  one  of 
the  most  simple  mechanical  problems,  and  one  which 
ensures  the  greatest  economy  of  fuel.  It  is  a  curious 
fact  that  although  economy  of  fuel  is  regarded  by  the 
Government  as  of  great  national  importance,  no  effort 
has  been  made  to  instruct  the  public  on  these  simple 
facts.  That  their  desire  to  give  instruction  is  very 
great  is  evidenced  by  the  fact  that  recently  thousands 


GOUT    AND    THE    LITHIC    DIATHESIS     139 

of  pounds  were  expended  on  advertisements  directing 
the  public  not  to  poke  the  fire  ! 

Having  regard  to  the  great  importance  of  this  subject, 
I  made  a  series  of  experiments  as  to  the  actual  amount 
of  coal  gas  necessary  to  heat  the  largest  dwelling-rooms 
when  practically  the  whole  of  the  heat  was  utilized, 
partly  as  radiant  heat,  and  partly  as  convected  heat. 
I  found  that  a  small  six-burner  gas  stove  using  10  to 
12  cubic  feet  of  gas  per  hour  was  not  only  ample,  but 
more  efficient  than  the  ordinary  gas-fire  burning  30  feet 
of  gas  per  hour.  I  accomplished  this  by  making  the 
stove  independent  of  the  flue  pipe  or  chimney  for  its 
draught,  so  that  it  was  no  longer  necessary  for  60  per 
cent  of  the  heat  to  escape  up  the  chimney.  But  I  found 
that  the  whole  subject  of  domestic  heating  involved 
huge  commercial  interests,  and  reform  is  difficult.  It 
is  ridiculous  to  talk  of  fuel  economy  while  the  present 
conditions  remain,  nor  is  it  possible  to  have  properly- 
heated  rooms  when  radiant  heat  alone  is  used. 

Next  to  warm  underclothing  and  properly  warmed 
rooms  as  a  means  of  preventing  gout  and  rheumatism, 
I  attach  great  importance  to  the  body  being  well  pro- 
tected from  loss  of  heat  during  the  night.  On  the 
Continent  the  '  duvet '  used  to  cover  the  body  during 
sleep  is  exceedingly  light,  but  possesses  the  power  of 
checking  the  radiation  of  heat  from  the  body  much  more 
efficiently  than  the  blankets  used  in  this  country,  and 
is  sufficient  to  maintain  the  action  of  the  skin  during 
rest.  I  was  puzzled  at  one  time  to  account  for  the  fact 
that  in  Germany,  where  the  consumption  of  nitrogenous 
food  is  greater  than  in  this  country,  and  beer  is  drunk 
in  large  quantities,  and  the  climate  is  less  equable, 
gout  was  less  prevalent  than  in  this  country.  Apart 
from  the  fact  that  nitrogenous  foods  are  not  directly 


140     GOUT    AND    THE    LITHIC    DIATHESIS 

concerned  in  the  production  of  uric  acid,  and  the  rooms 
are  better  warmed,  I  believe  that  the  gigantic  down 
'  duvets '  under  which  they  sleep,  and  perspire,  are  the 
real  solution  of  the  question. 

Another  important  factor  in  the  formation  of  lithates 
is  the  lack  of  fluidity  in  the  lymph  and  secretions.  This 
may  be  due  to  the  simple  fact  that  the  person  does 
not  drink  enough  fluid.  In  some  of  the  most  marked 
cases  I  have  met  with  of  this  deficiency,  the  patient 
had  been  advised  never  to  drink  at  meals,  in  order  to 
improve  digestion.  The  result  was  that  no  drink  was 
taken  either  before  or  after  the  meal,  and  the  total 
amount  of  fluid  consumed  in  the  day  was  much  below 
the  normal  requirements  of  the  body.  In  these  cases 
both  the  blood  and  the  lymph  become  thickened. 
This  causes  a  difficulty  in  the  blood  finding  its  way 
through  the  small  capillary  blood-vessels,  and  such 
patients  often  present  the  appearance  of  anaemia,  the 
complexion  having  a  dark,  pallid  hue.  In  many  cases 
I  have  found  that  these  patients  had  been  actually 
treated  by  iron  tonics,  with  the  result  that  headache 
and  congestion  were  produced.  If  we  take  the  specific 
gravity  of  the  blood  in  these  cases,  it  is  frequently  above 
1060  and  has  a  high  degree  of  coagulability.  In  some 
cases  the  embarrassment  of  the  heart  has  been  so  great 
that  heart  tonics  have  been  used  over  a  considerable 
period,  without  satisfactory  results.  I  have  cured  a 
number  of  such  cases,  where  the  gravest  prognosis  has 
been  given,  with  no  other  remedy  than  home-made 
lemonade  in  large  doses. 

I  have  long  distrusted  my  own  judgement  in  the 
diagnosis  between  anaemia  and  haemoglobin  excess, 
and  never  give  an  opinion  without  examination.  This 
can  be  done  in  a  few  minutes  by  placing  a  drop  of 


GOUT    AND    THE    LITHIC    DIATHESIS     141 

the  patient's  blood  in  a  mixture  of  chloroform  and 
benzene,  and  then  adding  more  of  the  one  or  other 
ingredient  until  the  fluid  is  of  the  same  specific  gravity 
as  the  drop  of  blood.  The  specific  gravity  of  the  fluid, 
taken  with  an  ordinary  urinometer,  will  then  give  the 
specific  gravity  of  the  blood.  Allowing  for  the  variation 
of  individual  constitutions,  we  usually  find  a  higher 
specific  gravity  in  patients  of  the  lithic  diathesis  -than 
we  do  in  those  of  the  lactic-acid  diathesis.  In  rheumatic 
patients  it  is  usually  very  low,  and  this  will  explain 
the  lack  of  oxidizing  power  in  such  cases. 

Contrary  to  expectation,  I  have  found  many  patients 
who  live  upon  a  fruit  and  vegetable  diet  largely,  who 
have  sometimes  a  pallid  appearance,  have  a  normal 
specific  gravity  of  the  blood  with  a  full  proportion  of 
haemoglobin.  In  addition  to  the  importance  of  obtain- 
ing the  necessary  fluidity  of  the  blood  and  lymph  in 
lithic  patients,  the  question  of  the  amount  of  haemo- 
globin is  important  in  reference  to  diet.  The  patient 
with  blood  of  a  high  specific  gravity  is  better  without 
too  much  meat,  because  it  increases  the  haemoglobin, 
which  is  already  in  excess. 

The  water  consumed  b.y  lithic  patients  who  live  in 
districts  where  the  water  contains  much  lime  is  better 
boiled  to  get  rid  of  the  excess.  There  is  no  doubt  that 
hard  water,  especially  in  some  districts,  increases  the 
tendency  to  the  production  of  lithates.  On  the  other 
hand,  water  with  an  absence  of  lime  favours  the  pro- 
duction of  true  rheumatoid  arthritis.  Therefore,  for 
ordinary  use,  I  do  not  think  that  distilled  water  is 
always  advisable,  even  if  the  water  is  very  hard.  It 
usually  results  in  too  little  fluid  being  taken,  and 
is  not  always  fresh  unless  prepared  at  home. 

While  the  lithic  patient  has  generally  a  good  digestion, 


142      GOUT    AND    THE    LITHIC    DIATHESIS 

he  is  more  likely  than  others  to  suffer  from  those 
digestive  disturbances  due  to  the  consistency  of  the 
bile  being  too  thick,  so  that  there  is  delay  or  irregularity 
in  its  passage  through  the  gall-duct.  Such  patients 
may  have  periodic  attacks  of  headache  or  bilious 
attacks,  and  in  some  cases  may  have  severe  pain  in  the 
gall-duct,  or  even  the  formation  of  gall-stones.  Pain 
in  the  gall-duct  is  often  referred  to  the  region  of  the 
appendix,  and  many  cases  diagnosed  as  appendicitis 
are  due  to  this  cause.  Such  attacks  are  usually  recur- 
rent. In  the  intervals  there  may  be  a  good  deal  of 
distention  in  the  upper  part  of  the  abdomen.  For  the 
relief  of  this  condition  I  have  found  a  pill  composed  of 
ext.  belladonna?  gr.  \,  podophylli  resina  gr.  J,  with  or 
without  aloin  gr.  ^,  act  as  specific  if  taken  regularly 
twice  or  three  times  a  week.  But  it  is  important  in 
such  cases  that  a  good  supply  of  fluid  should  form  an 
essential  part  of  the  diet. 

I  have  discussed  in  a  previous  chapter  the  chemical 
changes  which  lead  to  the  formation  of  the  insoluble 
lithates.  We  have  now  to  consider  the  physiological 
conditions  which  cause  the  lithates  to  undergo  chemical 
changes  and  produce  the  symptoms  called  gout. 

We  have  to  remember  that  every  mass  of  lithates  is 
in  a  state  of  cohesion  with  the  living  cell.  We  know 
that  the  cell-wall  of  the  living  cell  can  receive  and  dis- 
charge lactic  acid  without  producing  any  symptoms, 
and  that  the  process  is  constantly  taking  place  under 
normal  conditions. 

Prior  to  the  attack  of  gout  there  must  be  a  large 
accumulation  of  lactic  acid  in  the  living  cell-wall,  and 
when  this  is  suddenly  liberated  by  heat  or  active  exer- 
cise, and  there  is  mechanical  interference  to  its  passage 
to  the  lymph-space  by  the  presence  of  the  lithic  con- 


GOUT    AND    THE    LITHIC    DIATHESIS      143 

cretion  and  the  density  of  the  surrounding  tissue,  some 
of  it  must  combine  with  the  alkaline  lithates  and  cause 
a  certain  amount  of  softening  and  decomposition.  It 
will  be  observed  that  the  causes  of  the  acute  attack — 
heat  and  physical  exercise — are  just  the  reverse  of  those 
which  lead  to  the  production  of  the  lithate  itself.  The 
symptoms  produced  by  the  addition  of  the  acid  to  the 
lithate  will  vary  with  the  amount  added.  We  may 
have  merely  slight  tenderness  or  pain  coming  on  at 
night  from  the  warmth  of  the  bed,  and  disappearing 
in  the  morning,  or  we  may  have  various  degrees  of 
pain  up  to  the  classical  acute  attack. 

The  primary  effect  of  the  addition  of  lactic  acid  is 
slightly  to  increase  the  bulk  and  soften  the  surface  of 
the  mass.  This  can  be  recognized  if  we  manipulate  the 
joint  during  the  early  symptoms  of  a  subacute  attack. 
The  interference  with  the  normal  alkalinity  of  the 
lithate  excites  a  certain  amount  of  irritation  of  the 
living  cells  with  which  it  is  in  contact,  and  this  causes 
an  increased  flow  of  blood  to  the  part,  with  effusion  of 
lymph.  The  result  is  a  solvent  action  on  the  periphery 
of  the  mass.  There  is  increased  heat  in  the  part 
affected,  with  consequent  further  liberation  of  lactic 
acid,  which  excites  more  inflammatory  action,  and 
increased  decomposition  of  the  lithates. 

The  whole  process  can  be  observed  in  those  cases 
where  the  mass  of  lithates  affected  are  only  covered 
by  the  skin.  It  will  be  noticed  that  the  mass  is  the 
centre  of  an  inflammatory  area,  where  great  effusion 
of  lymph  has  taken  place.  The  periphery  of  the 
mass  of  lithates  becomes  softer  and  finally  has 
the  consistency  of  milk,  and  absorption  of  the  fluid 
is  taking  place  and  the  mass  becomes  smaller.  At 
first,  the  centre  of  the  mass  retains  its  normal  chalklike 


144     GOUT    AND    THE    LITHIC    DIATHESIS 

consistency ;  but,  as  the  attack  continues,  the  whole 
mass  becomes  softer.  It  looks  now  as  if  the  mass  would 
be  dissolved  and  disappear ;  but  I  have  never  seen 
this  happen.  At  this  stage  the  attack  suddenly  ceases, 
the  inflammation  subsides,  the  effusion  disappears, 
and  what  is  left  of  the  lithates  resumes  its  normal 
consistency- 

This  appears  to  offer  conclusive  proof  that  the 
exciting  cause  of  the  attack  cannot  exist  in  the  blood 
or  the  lymph.  If  it  did  so,  the  attack  would  continue 
until  the  whole  of  the  lithate  was  removed,  as  in  the 
cases  when  other  peccant  matters  set  up  inflammation 
and  the  blood-cells  are  concerned  in  their  removal. 
If  the  blood  contained  the  cause  which  excites  the 
attack,  all  lithates  would  undergo  the  same  process  of 
decomposition  simultaneously ;  but,  as  I  have  pointed 
out,  this  does  not  occur.  Masses  of  lithate  in  other 
joints  are  wholly  unaffected  by  the  process,  no  matter 
how  long  it  may  continue. 

The  whole  evidence  shows  that  the  exciting  cause 
of  the  chemical  action  is  local,  and  that  the  quantity 
is  limited,  and  becomes  itself  destroyed  b}'  the  process. 
The  inflammation  caused  by  the  attack  of  gout  not  only 
liberates  lactic  acid  from  the  surrounding  cell-walls, 
but  also  favours  its  elimination.  This  can  be  demon- 
strated by  testing  the  reaction  of  the  skin  over  a  joint 
during  the  attack.  It  will  be  found  to  be  intensely  acid  ; 
but  if  we  test  the  skin  reaction  some  six  inches  away 
from  the  joint,  it  may  only  show  a  very  slightly  acid 
reaction.  This  proves  not  only  that  the  attack  is 
liberating  acid  from  the  tissues,  but  also  how  localized 
is  the  action  of  the  skin  in  the  elimination  of  the  pro- 
ducts which  are  formed  in  the  tissues  immediately 
beneath  any  part  of  it.  It  is  for  this  reason  that  we 


GOUT    AND    THE    LITHIC    DIATHESIS     145 

obtain  different  reactions  of  the  skin  in  various  parts 
of  the  body,  even  under  normal  conditions. 

A  case  illustrating  this  point  came  recently  under 
my  observation.  An  elderly  lady,  of  robust  type,  had 
an  enormous  collection  of  lithates  round  the  finger- 
joints,  so  that  some  of  them  were  deformed,  bat  there 
was  a  singular  absence  of  lithates  in  all  the  other  joints 
of  the  body.  This  puzzled  me  very  much,  until  she  told 
me  that  many  years  ago  her  dress  caught  fire  and  she 
put  up  her  hands  to  save  her  face  from  being  burned  ; 
the  result  was  that  all  the  skin  of  the  back  of  both 
hands  and  fingers  was  completely  destroyed.  The  surface 
had  healed  in  a  remarkable  manner,  but  of  course  all 
the  sweat-ducts  on  the  dorsal  surfaces  were  destroyed. 
This  fully  explained  the  cause  of  her  trouble  and  its 
strict  localization. 

Of  course,  in  the  more  chronic  forms  of  gout,  where 
there  is  defective  excretion  of  lactophosphate  of  lime 
by  the  kidney,  the  condition  of  the  blood  which  results 
must  exercise  some  influence  upon  the  frequency  and 
duration  of  the  attack,  as  it  does  upon  the  general 
health. 

In  my  experiments  with  lactophosphate  of  lime  I 
found  that  to  produce  'uric  acid'  we  required  two 
reagents,  an  acid  and  oxygen.  Under  normal  con- 
ditions neither  of  these  agents  will  produce  any  effect 
upon  the  oxidized  lactophosphate  of  lime  which  forms 
the  lithates  ;  but  when  chemical  transformation  has 
commenced,  the  lithate  irritates  the  living  cells  to  which 
it  is  attached,  and  these  cells  are  influenced  by  the 
condition  of  the  lymph  which  surrounds  them.  This 
will  explain  the  fact  that  a  person  whose  joints  may 
be  crowded  with  lithates  can  eat  red  meat  and  take 
acid  drink  without  the  slightest  symptom  being  pro- 

10 


146     GOUT    AND    THE    LITHIC    DIATHESIS 

duced,  and  will  benefit,  whilst  the  patient  with  lithates 
in  a  state  of  painless  decomposition  may  experience 
almost  immediate  pain  from  some  acid  drink  or  in- 
creased act  of  oxidation. 

But  this  condition  does  not  occur  unless  the  tissues 
are  loaded  with  lactic  acid  to  the  saturation  point  and 
there  is  a  physiological  obstacle  to  its  elimination. 
Directly  such  patients  have  a  free  action  of  the  skin 
and  elimination  of  the  lactic  acid,  they  can  take  red 
meats  and  acids  with  impunity.  For  this  reason  I 
have  practically  never  occasion  to  diet  patients  when 
under  my  treatment.  They  make  the  best  recoveries 
when  they  abandon  strict  dietary  and  take  ordinary 
food. 

Thus  a  gentleman,  accustomed  all  his  life  to  drink 
port  wine  at  dinner,  and  who  also  took  regular  daily 
exercise,  had  a  first  attack  of  rheumatic  gout  in  a  number 
of  joints  at  the  age  of  eighty.  He  was  treated  for  this 
at  a  spa,  where  abstinence  from  wine  was  part  of  his 
regime.  His  joints  were  unrelieved,  and  his  health 
suffered  seriously,  and  he  came  to  me  in  a  very  weak 
state.  I  at  once  restored  his  port  wine,  gave  him  daily 
baths,  and  he  made  a  complete  recovery. 

The  port-wine-drinking  habits  of  our  ancestors  as  a 
cause  of  gout  is  a  delusion  firmly  rooted  in  the  public 
mind.  It  is  forgotten  that  the  labouring  classes  in 
those  days  drank  large  quantities  of  strong  beer  and 
did  not  develop  gout ;  yet  beer  is  regarded  as  quite  as 
potent  a  cause  of  gout  as  port  wine.  Gout  was  the 
aristocratic  disease  because  it  affected  those  who  did 
not  earn  their  bread  by  physical  labour.  It  was  not  the 
port  which  caused  gout,  but  the  fact  that  our  ancestors 
neither  took  baths  nor  kept  their  skins  clean  by  the 
sweat  of  physical  exertion.  If  we  examine  any  large 


GOUT    AND    THE    LITHIC    DIATHESIS     147 

mansion  built  a  century  ago,  we  shall  find  that  no 
provision  was  made  for  a  bath-room  ;  the  necessity  for 
it  never  occurred  to  the  architect.  The  skin  under 
such  conditions  would  be  so  coated  with  dead  cells  that 
it  could  no  longer  become  an  organ  of  excretion,  and  so 
we  had  gout  of  a  more  active  type  than  is  known  at 
the  present  day,  when  baths  are  regarded  as  necessary 
to  civilization. 

The  question  of  alcohol  in  relation  to  gout  has  been 
discussed  without  any  relation  to  the  fact  that  alcohol 
may  act  as  a  direct  stimulant  to  the  tissues  and  the 
processes  of  metabolism,  or  as  a  cause  of  exhaustion, 
according  to  the  doses  which  may  be  taken.  We  have  to 
remember  that  a  large  proportion  of  the  inhabitants  of 
this  country  have  a  persistent  subnormal  temperature, 
and  this  is  the  direct  cause  of  gouty  and  arthritic 
troubles.  One  of  the  most  important  physiological 
and  therapeutic  questions  which  concern  the  medical 
profession  is  to  find  some  remedy  which  will  restore 
the  subnormal  temperature.  By  doing  so  they  would 
arrest  the  cause  of  a  large  amount  of  the  disease  and 
debility  from  which  the  British  public  suffer.  I  have 
been  working  at  this  subject  during  the  last  thirty 
years,  and  have  failed  to  discover  any  agent  except 
alcohol  in  moderate  doses  which  can  permanently  raise 
the  body  temperature. 

I  am  fully  aware  that  writers  have  stated  repeatedly 
that  alcohol  lowers  the  temperature,  but  I  have  found 
no  experimental  work  to  justify  this  statement.  I  am 
not  concerned  with  the  immediate  effect  of  a  dose  of 
alcohol — this  in  any  case  must  be  very  transient — but 
of  the  use  of  alcohol  in  small  doses  once  or  twice  daily 
with  the  meals,  over  a  period  of  some  weeks.  My 
experiments  show  that  in  a  large  proportion  of  cases 


148     GOUT   AND  THE     LITHIC    DIATHESIS 

where  the  temperature  is  subnormal  the  effect  of 
alcohol,  used  in  this  way,  is  to  raise  the  temperature 
permanently.  The  results  may  not  appear  on  the 
temperature  chart  for  some  days  after  the  course  has 
been  commenced,  and  in  every  case  it  is  gradual.  This 
shows  that  it  is  not  the  direct  stimulant  action  of 
alcohol  which  produces  the  result.  It  must  have  a 
definite  food  value  in  increasing  the  metabolic  processes 
oftthe  body. 

I  have  tried  to  discover  some  other  agent  which  will 
give  the  same  result,  but  so  far  I  have  failed.  I  wish 
it  were  otherwise.  I  am  quite  certain  that  if  prohibition 
were  adopted  in  this  country  there  would  be  a  great 
increase  in  the  number  of  patients  of  the  arthritic 
class,  and  probably  a  century  would  elapse  before  the 
cause  was  discovered. 

I  think  it  quite  possible  that  the  excessive  use  of 
alcohol  may  cause  or  contribute  to  the  production  of 
arthritic  disorders,  because  over-stimulation  must  pro- 
duce exhaustion  ;  but  I  have  had  a  singular  absence  of 
evidence  on  this  point  in  my  personal  experience.  On 
the  other  hand,  I  have  been  struck  by  the  fact  that 
the  large  majority  of  patients  I  have  to  treat,  either 
take  no  alcohol  at  all  or,  if  they  do  so,  take  it  in  very 
moderate  quantities.  I  have,  however,  seen  a  good 
many  cases  where  gout  could  be  directly  attributed 
to  excess  in  food,  and  some  of  the  worst  offenders  in 
this  respect  were  men  who  boasted  that  they  had 
been  life-long  abstainers  and  never  smoked.  I  think 
smoking  has  one  beneficial  effect :  those  who  indulge 
most  do  not  consume  too  great  a  quantity  of  food. 

When  we  are  treating  a  patient  with  the  lithic 
diathesis  our  object  is  to  increase  the  production  of 
lactic  acid,  set  it  free  from  the  tissues,  and  ensures  its 


GOUT    AND    THE   LITHIC  DIATHESIS       149 

elimination.  This  we  can  do  in  robust  men  by  active 
exercise  under  conditions  which  produce  free  action  of 
the  skin.  But  if  we  try  the  method  on  those  who  are 
not  so  robust,  we  shall  cause  fatigue,  which  is  a  factor 
to  be  avoided.  Moderate  exercise  with  pyretic  treat- 
ment gives  better  results  in  these  cases.  In  subacute 
cases  of  lithitis  when  some  of  the  urates  are  being 
decomposed,  active  exercise  is  contra-indicated,  as  we 
do  not  need  any  surplus  of  lactic  acid  in  the  lymph. 
Pyretic  treatment  with  copious,  slightly  alkaline  drinks 
will  relieve  the  irritation.  Acids  and  acid  fruits  are  to 
be  avoided  only  during  the  duration  of  the  attack. 
To  deprive  the  lithic  patient  of  fruit  under  ordinary 
conditions  is  very  undesirable.  In  certain  cases,  sugar 
or  red  meats  will,  at  this  stage,  by  stimulating  oxidation, 
increase  the  pain  ;  but  these,  as  I  have  mentioned, 
will  only  do  so  while  the  cells  are  overloaded  with 
lactic  acid.  Directly  we  relieve  this,  they  can  be  taken 
with  advantage. 


150 


CHAPTER    XI. 

'ARTHRITIS.' 

DURING  recent  years  this  word  has  been  used  to 
designate  joint  diseases  of  a  widely  different  character, 
so  that  it  has  ceased  to  convey  any  information  as  to  the 
pathological  condition  present,  or  afford  any  guide  to 
prognosis  or  treatment.  Thus,  in  Sarjous'  Analytical 
Cyclopedia  of  Practical  Medicine  I  find,  under  the  head- 
ing, '  Chronic  Rheumatism ',  chronic  articular  rheumatism 
or  rheumatoid  arthritis,  rheumatic  gout,  rhumatisme 
chronique  infectieux,  polyarthritis  deformans,  and 
osteo-arthritis.  This  disease,  which  has  received  so 
many  names,  is  stated  to  be  '  due  in  all  probability  to 
the  invasion  of  micro-organisms'.  We  have  here  a 
number  of  forms  of  joint  disease,  differing  in  their 
etiology,  pathology,  and  treatment,  classified  as  one 
disease  and  due  to  the  same  cause.  It  is  not  remark- 
able, under  such  conditions,  that  treatment  fails  and 
a  grave  prognosis  is  given  in  every  case.  The  names 
in  common  use  will  do  well  enough  to  describe  the 
cases  met  with  in  daily  practice. 

CHRONIC     RHEUMATISM. 

This  is  a  disorder  found  in  persons  of  a  sound 
constitution  and  who  are  often  robust.  The  patient 
may  be  of  the  lactic-acid  diathesis,  or  have  been  in  the 
habit  of  producing  large  quantities  of  lactic  acid  as  a 
result  of  physical  exertion.  Thus  the  labourer  in  the 
fields  is  liable  to  suffer  from  chronic  rheumatism,  while 


CHRONIC  RHEUMATISM  151 

his  master,  the  squire,  under  different  physical  con- 
ditions, is  troubled  with  gout.  Chronic  rheumatism  is 
much  more  likely  to  attack  those  whose  skin  excretion 
is  unusually  active.  Thus  a  person  resident  in  a  hot 
climate,  where  excessive  action  of  the  skin  is  produced 
by  the  heat,  will,  on  returning  to  this  country,  have  a 
check  given  to  the  cutaneous  excretion,  and  may  as  a 
result  develop  chronic  rheumatism  and  become  an 
absolute  cripple  for  life  because  the  cause  is  not  under- 
stood. 

The  cause  of  chronic  rheumatism  is  a  chill  which 
checks  the  excretion  of  the  skin,  no  reaction  taking 
place.  It  may  be  difficult  to  understand  the  failure  of 
reaction  in  persons  who  are  frequently  robust,  but 
clinical  experience  shows  that  the  condition  may  con- 
tinue for  years  without  reaction  occurring.  When  it 
does  occur  we  have  the  symptoms  of  rheumatic  fever, 
which  is  the  natural  method  of  cure.  But  in  cases  of 
chronic  rheumatism,  if  we  raise  the  temperature  arti- 
ficially we  can  seldom  produce  a  continued  pyrexia  of 
an  active  character  ;  the  daily  rise  may  be  only  two  or 
three  degrees  above  the  patient's  normal ;  in  many 
cases  no  continued  rise  of  temperature  takes  place,  in 
spite  of  daily  treatment.  This  indicates  that  the 
lactic  acid  in  the  cell-wall  is  in  a  state  of  chemical 
combination  with  the  lactophosphate  of  lime,  whereas 
under  ordinary  conditions  a  large  part  of  the  lactic 
acid  is  simply  additive  and  easily  liberated  by  a  rise 
of  temperature. 

Chronic  rheumatism  has  certain  diagnostic  symptoms 
which  clearly  distinguish  it  from  other  forms  of  chronic 
joint  disease.  If  we  examine  the  hand,  we  shall  find 
that  the  fingers  are  partially  flexed  without  any  swell- 
ing of  the  joints.  The  knuckles  will  probably  appear 

CQLLlEGl 

l-  K  \  s  I  e  i  -  , 


152  ARTHRITIS 

swollen,  but  closer  examination  will  show  that  this  is 
due  to  wasting  of  the  muscles  and  the  tissues  round 
the  joints.  The  muscles_waste  in  chronic  rheumatism 
because  the  joints  are  disused,  and  also  on  account  of 
the  thickening  of  the  cell- walls  interfering  with  nutrition. 
The  latter  factor  is  important,  and  has  never  been 
pointed  out.  Although  the  muscles  have  wasted,  they 
retain  their  resiliency  and  are  firm  on  pressure.  We 
find  as  the  case  goes  on  that  both  the  elbows  and  knees 
become  flexed  and  movement  is  considerably  impaired. 
The  arms  become  increasingly  less  capable  of  abduction 
and  of  being  raised  to  the  head,  because  of  the  stiffening 
of  the  shoulder- joint. 

In  some  cases  we  may  find  symptoms  which  appear 
to  justify  the  diagnosis  of  'rheumatoid  arthritis'.  Some 
of  the  small  joints  of  the  fingers  may  be  ankylosed,  or 
have  undergone  such  destructive  changes  that,  instead 
of  flexion,  we  have  a  slight  backward  displacement,  so 
that  a  concavity  appears  over  the  dorsal  surface  of  the 
joint.  But  this  differs  from  rheumatoid  arthritis  in 
the  fact  that  it  is  not  the  commencement  of  general 
destructive  changes  in  the  joints,  but  a  purely  local 
disturbance  which  is  not  likely  to  be  repeated  during 
the  lifetime  of  the  patient.  We  may  also  find  in 
advanced  cases  a  slight  abduction  of  the  hand  from  the 
wrist,  due  to  muscular  atrophy.  This  disappears  as 
the  patient  recovers.  In  some  cases  there  is  synovitis 
of  the  knee-joints  due  to  secondary  symptoms  or  over- 
strain of  the  joint,  but  this  does  not  alter  the  fact  that 
swelling  of  the  joints  is  not  a  normal  symptom  of 
chronic  rheumatism. 

Although  the  symptoms  of  this  disorder  are  so 
characteristic,  I  have  not  seen  a  chronic  case  for  many 
years  which  has  not  been  diagnosed  as  rheumatoid 


-.  J  H  ?>  K  f 


CHRONIC   RHEUMATISM  153 

arthritis  and  received  the  treatment  and  prognosis  of 
that  disease. 

Long  clinical  experience  enables  me  to  affirm  that 
chronic  rheumatism  is  a  curable  disease,  even  when  it 
has  existed  for  many  years.  Such  cases  involve  much 
time  and  trouble,  because  it  is  necessary  to  treat  not 
only  the  disease  but  the  physiological  and  physical 
consequences.  Chronic  rheumatism  is  wholly  due  to 
physical  causes,  and  can  only  be  treated  by  physical 
agents  which  overcome  the  condition.  It  is  in  such 
cases  that  wrong  diagnoses  and  the  bacteriological 
theory  have  done  an  extraordinary  amount  of  harm 
to  humanity.  Not  only  are  vaccines  useless  in  such 
cases,  but  they  waste  valuable  time,  during  which  the 
disease  is  making  progress,  and  debilitate  the  patient 
when  he  needs  all  his  powers  of  vital  resistance. 

The  following  case  will  illustrate  chronic  rheumatism 
in  its  most  simple  form,  both  as  regards  its  cause  and 
cure  : — 

A  lady  of  middle  age,  and  of  a  robust  type,  had  lived 
most  of  her  life  in  South  America,  in  a  very  hot  climate, 
where  she  had  excessive  action  of  the  skin.  She  came 
to  this  country  five  years  ago.  She  was  chilled  by  the 
cold  and  damp,  and  began  to  develop  stiffness  and  pain 
in  her  joints.  This  increased  very  gradually  until  her 
fingers  had  become  flexed  so  that  she  could  use  them  but 
little  ;  but,  being  a  very  energetic  woman,  she  tried  to 
use  all  her  joints  in  spite  of  their  stiffness.  Her  case 
was  diagnosed  as  rheumatoid  arthritis,  and  under 
advice  she  had  all  her  teeth  removed,  in  spite  of  the 
fact  that  they  were  perfectly  sound.  This,  of  course, 
did  not  help  her,  and  after  varied  treatment  she  con- 
sulted me.  The  case  was  one  of  typical  chronic 
rheumatism,  and  I  ordered  pyretic  treatment,  which  I 


154  ARTHRITIS 

considered  would  meet  all  the  requirements  of  her  case. 
I  did  not  see  her  again  for  four  weeks,  and  she  told 
me  she  had  only  eight  treatments  owing  to  domestic 
difficulties  ;  but  I  was  astonished  at  the  extraordinary 
change  in  her  physical  condition  :  the  stiffness  had 
gone  from  her  joints,  and  she  was  able  to  move  her 
fingers  freely,  and  this  had  happened  in  a  much  shorter 
time  than  I  expected. 

The  nurse  who  gave  the  treatment  told  me  that 
during  the  first  six  treatments  the  patient  exfoliated 
an  enormous  quantity  of  epithelial  scales.  It  is  evident 
that,  the  action  of  the  skin  being  checked,  the  dead 
cells  had  remained  on  the  skin,  forming  an  impermeable 
coating  and  an  entire  check  to  excretion.  The  treat- 
ment had  set  free  the  necessary  lactic  acid  to  remove 
this  coating,  which  could  not  have  been  removed  by 
hot  baths  or  soaps.  The  patient  was  naturally  healthy, 
and  the  restoration  of  her  skin  to  a  condition  which 
enabled  it  to  perform  its  natural  functions  enabled  her 
to  clear  out  the  excess  of  lactic  acid  from  the  cell-walls. 
In  this  case  the  power  of  vital  resistance  of  the  patient 
was  a  great  factor  in  the  early  success  of  the  treatment. 

Another  case,  which  I  have  at  present  under  treat- 
ment, well  illustrates  the  unfortunate  results  of  failure 
of  diagnosis,  combined  with  the  bacteriological  theory. 
It  will  be  understood  that  I  never  blame  the  practitioner 
in  these  cases,  because  his  only  sources  of  reference  do 
not  provide  him  with  the  means  of  differentiation,  and 
lead  him  to  adopt  a  theory  which  is  unsupported  by 
either  pathological  or  clinical  evidence. 

The  patient  was  a  healthy  man  who  had  not 
been  away  from  business  through  illness  for  twenty 
years.  He  then  had  a  slight  attack  of  rheumatism, 
which  was  regarded  as  due  to  auto-infection  and 


CHRONIC  RHEUMATISM  155 

promptly  treated  by  vaccine.  On  the  other  hand, 
there  was  a  distinct  history  of  malaise  for  six  months 
before  the  attack.  The  patient  felt  tired  by  his  work, 
had  a  strong  indisposition  to  take  exercise,  and  used 
his  motor  to  go  to  the  station  instead  of  walking.  The 
symptoms  were  those  I  have  described  as  the  precursors 
of  the  rheumatic  attacks.  The  following  is  the  report 
sent  me  by  his  medical  adviser  : — 

"At  the  end  of  1913,  and  in  January,  1914,  Mr.  X 
complained  of  pain  and  stiffness  of  toes.  Subsequently 
was  found  with  a  large  abscess  round  a  tooth.  In  1915 
had  abscess  in  throat.  Erythema  scarlatiniforme,  with 
arthritis  in  fingers,  toes,  and  ankle.  Had  vaccine  admin- 
istered. This  did  undoubted  good,  and  was  continued  up 
to  April,  1917.  lonization,  sod.  salicyl.,  and  vaccine  up 
to  July,  1917.  This  last  vaccine  did  not  do  much,  and 
seemed  to  upset  him.  Since  it  was  given  up,  a  long 
course  of  ionization,  massage,  etc.,  has  been  tried,  but  his 
illness  has  progressed  in  spite  of  all." 

The  following  is  the  patient's  report  of  his  illness  :  — 

"  First  symptoms,  pain  in  feet  like  pebbles  in  shoes; 
treated  by  Dr.  A.  with  medicine. 

"  1914.  Pain  down  leg  after  sitting  down.  Dr.  A. 
took  me  to  Dr.  B.,  who  made  vaccine  from  specimens 
(i.e.,  gums  and  faeces).  After  third  inoculation,  rash  all 
over  body,  throat  very  septic,  diagnosed  rheumatic  ery- 
thema. 

"  1915.  Continued  inoculation  with  Dr.  B.'s  vaccine 
for  about  six  months. 

"  1916.     Had  a  second  lot  of  Dr.  B.'s  vaccine. 

"  1917.  January:  Tonsils  were  taken  out,  as  they  were 
found  very  septic,  and  supposed  to  be  the  cause  of  my 
trouble.  On  fifth  da}'  after  first  tonsil  was  removed  had 
a  bad  haemorrhage  from  the  throat  and  nearly  went  West. 
After  some  weeks  had  second  tonsil  taken  out.  I  was  a 
long  time  recovering  from  this,  and  was  very  weak  for  a 
long  time. 

"  February  :  Had  vaccine  made  from  tonsils  by  Dr.  C. 
May  and  June  :  Had  a  second  lot  of  vaccine  made  by 
Dr.  C.  Developed  pains  in  shoulders  very  acutely. 
July  :  gave  up  vaccine,  and  by  end  of  August  was  very 
crippled  and  suffered  much  pain.  Then  went  to  Dr.  D., 


156  ARTHRITIS 

who  gave  high-frequency  for  pain,  which  did  some  good  ; 
then  ionization  for  some  months. 

"  1918.  Knees  very  bad ;  obliged  to  use  crutches. 
X-ray  treatment  on  knee,  but  no  good  result.  Another 
vaccine  by  Dr.  E.  Local  radiant  heat  and  massage  for 
couple  of  years. 

"  1919.  Went  to  American  osteopath  for  two  months. 
Treatment  very  severe,  knees  terribly  painful,  nerves  very 
bad  from  severity  of  treatment. 

"  1919.  Went  to  Dr.  F.,  who  ordered  me  to  walk. 
Ionization  every  day  for  eight  weeks.  Vaccine  twice  a 
week  for  sixteen  months.  Massage  four  days  a  week  for 
eleven  months. 

"  1920.  July  and  August  :  Ionization  by  Dr.  G. 
nine  weeks,  and  massage  four  days  a  week.  Thyroid 
gland  to  begin  at  15  gr.  per  da}-  and  work  up  to  45  gr. 
When  I  had  taken  30  gr.  per  day,  heart  got  bad  and  was 
very  depressed  and  nervous.  When  I  left  Dr.  G.,  he  had 
my  teeth  x-rayed  and  ordered  them  all  out.  This  I  did 
not  have  done.  Returned  to  Dr.  A.,  who  treated  me  for 
my  heart  and  nerves  and  recommended  me  to  Bath." 

I  have  reproduced  the  patient's  written  statement, 
only  substituting  letters  for  the  names  of  the  physicians 
attending.  The  condition  of  the  patient  on  arrival  was  : 
The  lower  limbs  were  contracted  to  an  angle  of  45°  and 
resisted  all  efforts  at  extension.  Both  elbows  were 
also  flexed.  The  shoulders  permitted  a  very  limited 
range  of  movement,  while  the  ankles  could  be  flexed 
and  extended  to  their  normal  degree.  The  fingers  were 
contracted  and  fixed,  so  that  they  could  not  be  extended 
or  fully  flexed.  Some  of  the  small  joints  showed  sym- 
ptoms of  degenerative  changes,  and  there  was  some 
abduction  of  the  whole  hand.  The  joints  were  not 
enlarged  or  swollen,  although  the  wasting  of  muscles 
gave  the  appearance  of  this  condition  existing.  My 
diagnosis  was  pure  'chronic  rheumatism'. 

It  will  be  noticed  that,  in  spite  of  the  fact  that  a 
source  of  auto-infection  was  discovered,  vaccines  used 
over  a  very  prolonged  period  proved  useless,  and  only 


CHRONIC   RHEUMATISM  157 

delayed  other  treatment.  The  practitioner  may  find 
sources  of  auto-infection  in  half  a  dozen  patients  a  day, 
who  have  not,  and  do  not,  develop  joint  trouble.  It 
is  only  when  such  trouble  commences  that  the  search 
is  made  for  this  source  as  a  cause  ;  and  if  this  investiga- 
tion fails,  then  the  bacteriologist  can  always  faU  back 
on  the  teeth,  as  few  people  have  teeth  beyond  reproach  ! 

The  treatment  adopted  in  this  case  and  other  similar 
cases  of  advanced  chronic  rheumatism  is  as  follows : — 

The  additive  lactic  acid  is  first  removed  by  daily 
pyretic  treatment.  This  is  continued  for  as  many 
weeks  as  the  excretion  of  the  skin  remains  acid.  Before 
all  the  acid  is  eliminated,  pain  during  rest  entirely 
ceases,  and  the  tissues  round  the  joints  are  softened, 
so  that  a  greater  range  of  movement  becomes  possible. 
This  is  increased  partly  by  passive  movement  and  also 
by  directing  the  patient  to  move  the  joint,  offering 
slight  resistance  to  the  movement,  and,  at  the  moment 
when  the  patient  has  completed  all  that  is  possible,  to 
him,  giving  such  assistance  as  will  increase  the  range 
of  movement. 

This  requires  great  caution,  because  it  is  quite  easy 
at  this  point  to  break  down  adhesions  and  cause  the 
patient  acute  pain ;  but  if  this  is  done  the  operator 
loses  the  confidence  of  the  patient,  and  it  will  be  difficult 
to  make  him  use  his  fullest  effort  to  move  the  joint 
again.  The  movement  of  assistance  should  be  given 
very  gently  and  slowly,  and  the  patient  should  be 
directed  to  call  out  directly  the  pain  becomes  too  great. 
If  the  operator  immediately  desists,  the  patient  will 
feel  confidence  and  will  submit  to  a  reasonable  amount 
of  pain  to  secure  greater  movement.  It  is  at  this  stage 
that  the  success  of  treatment  depends  very  much 
upon  the  efforts  of  the  patient.  It  is  for  this  reason 


158  ARTHRITIS 

that  the  pessimistic  prognosis  is  worse  than  the  lactic 
acid,  because  its  effects  are  frequently  more  difficult 
to  remove. 

I  recently  had  a  case  of  a  lady,  who  had  been  bed- 
ridden for  five  years  with  contracted  joints  as  a  result 
of  chronic  rheumatism.  It  had  been  so  impressed  upon 
her  that  she  had  'rheumatoid  arthritis'  and  was  incur- 
able, that  even  when  I  had  straightened  the  lower  limbs 
and  restored  the  use  of  the  knee-joints  she  would  lie 
with  them  in  the  flexed  position,  which  had  become 
their  most  natural  attitude,  and  refused  to  believe  that 
she  would  ever  walk  again.  It  was  not  until  I  had  put 
her  on  crutches,  and  taught  her  to  rise  from  a  chair 
without  assistance,  that  I  made  her  recognize  the 
possibility  of  walking.  From  that  moment  she  directed 
all  her  efforts  to  improving  her  powers  of  locomotion, 
and  recovered  rapidly. 

These  patients  have  nothing  to  do  but  improve  their 
range  of  movement  and  muscular  power,  and  they  must 
be  taught  the  best  way  of  doing  so. 

As  regards  the  shoulders,  the  ultimate  goal  is  to 
raise  the  elbow  as  high  as  the  top  of  the  head,  flex  the 
arm  over  the  head,  and  touch  the  ear  on  the  opposite 
side,  while  the  biceps  muscle  is  firmly  pressed  upon  the 
ear  of  the  sound  side.  They  can  begin  by  using  the 
hand  to  touch  the  mouth,  the  nose,  the  forehead,  and 
the  head,  always  striving  towards  the  final  result. 
Subsequently  they  should  be  taught  to  place  the  back 
of  the  hand  of  the  affected  side  on  the  sacrum,  and 
gradually  raise  it  up  the  spine  until  the  dorsal  region 
is  reached,  keeping  the  hand  in  contact  with  the  spine. 
When  these  two  movements  are  accomplished  the 
shoulder  has  resumed  its  functions. 

For  the  elbow,  the  patient  should  be  taught  to  make 


CHRONIC   RHEUMATISM  159 

efforts  to  touch  the  shoulder  with  the  tips  of  the  fingers, 
and  then  extend  the  arm  vigorously,  at  the  same  time 
separating  the  fingers  as  widely  as  posisble.  He 
should  also  make  movements  of  pronation  and  supina- 
tion  of  the  hand. 

The  wrist  is  most  conveniently  exercised  by  placing 
the  arm  palm  downwards  on  a  small  bedside  table,  so 
that  the  hand  from  the  wrist  projects  beyond  the  edge 
of  the  table.  The  patient  can  fix  the  wrist  himself, 
while  he  allows  the  hand  to  drop  as  far  as  possible  and 
then  raises  it  to  the  straight  position.  Subsequently 
he  performs  the  same  movement  with  a  small  book 
held  in  the  hand  to  give  resistance  to  the  extension 
movement. 

The  small  joints  of  the  fingers  should  be  exercised 
constantly  by  efforts  to  make  a  fist  and  then  extend 
the  fingers  as  widely  as  possible.  A  rubber  ring 
pessary  is  often  useful  in  cases  where  the  flexor  muscles 
require  exercise. 

The  muscles  of  the  hip-joint  can  be  exercised  by  the 
operator  holding  his  hand  on  a  level  with  the  top  of 
the  patient's  toes,  and  then  directing  him  to  move  the 
foot  in  a  circle  round  it  ;  then  to  perform  the  same 
movement  as  if  the  hand  was  there. 

For  the  knee-  and  ankle-joints,  flexion  and  extension 
movements  should  be  constantly  performed  so  far  as 
possible.  Even  if  the  range  of  movement  is  very 
limited,  the  effort  is  valuable,  as  it  stimulates  the  nerve 
centres  and  the  nerves  and  increases  their  blood-supply. 

It  is  not  advisable  to  allow  more  than  six  movements 
of  any  joint  to  be  made  at  one  time,  especially  in  the 
early  stages  ;  but  these  may  be  repeated  five  or  six 
times  a  day,  so  that  the  patient  who  means  to  get  well 
is  kept  fully  employed  without  undue  fatigue. 


160  ARTHRITIS 

I  very  seldom  think  it  desirable  to  break  down 
joints  under  an  ansesthetic.  In  some  cases,  where  the 
joint  has  no  movement  owing  to  contraction  and 
thickening  of  the  structures  round  it,  it  can  be  done 
with  advantage ;  or,  if  it  is  found  impossible  by 
means  of  extension  splints  to  straighten  a  limb  beyond 
a  certain  point  owing  to  the  strength  of  the  adhesions, 
force  may  be  required.  But  otherwise  there  is  little 
advantage  in  obtaining  a  greater  range  of  movement 
in  a  joint  than  the  muscles  can  control.  This  is 
especially  the  case  with  the  knee-joint.  A  patient 
may  be  able  to  walk  with  a  slightly  flexed  joint,  but 
be  whoUy  unable  to  do  so  if  the  joint  is  straightened 
before  the  muscles  are  able  to  give  the  necessary  support. 
In  many  cases  of  chronic  rheumatism,  even  when  the 
functions  of  the  knee  have  been  restored,  the  muscles 
may  be  too  wreak  'to  permit  the  patient  to  stand,  and  it 
is  necessary  to  use  a  splint  to  support  the  knee  when 
the  patient  begins  to  walk. 

This  happened  with  the  patient  whose  case  I  have 
described.  After  all  the  joints  had  been  restored  b}' 
the  methods  mentioned,  the  patient  was  able  to  walk 
on  crutches;  but  owing  to  the  extreme  wasting  of 
the  muscles  it  was  necessary  to  support  the  knees 
with  splints.  It  may  be  many  weeks  before  the  powers 
of  locomotion  are  restored.  I  always  dismiss  the 
patients  when  they- have  reached  this  stage. 

There  is  a  type  of  chronic  rheumatism  which  differs 
from  the  pure  form  I  have  described  because  it  is 
attended  b)'  great  debility.  It  is  usually  accompanied 
by  a  moist  acid  condition  of  the  skin  which  gives  no 
relief  to  the  symptoms.  These  cases  usually  occur  as 
secondary  to  rheumatic  fever,  and  convey  the  idea  that 
while  in  ordinarv  chronic  rheumatism  the  lactic  acid 


CHRONIC  RHEUMATISM  161 

is  locked  up  in  the  cell-walls  in  an  additive  form,  these 
have  a  large  amount  of  free  lactic  acid  which  excites 
excretion  without  the  full  functions  of  the  skin  being 
exercised.  Under  pyretic  treatment  the  sweat  is 
intensely  acid,  and,  as  this  free  acid  is  removed,  the 
tendency  to  passive  excretion  ceases.  In  these  cases 
pyretic  treatment  frequently  causes  a  temporary 
continued  rise  of  temperature,  which  is  a  mild  attack 
of  rheumatic  fever,  and  in  such  cases  the  period  of 
treatment  is  shortened. 

The  symptoms  in  these  cases  very  closely  resemble 
rheumatoid  arthritis,  because  of  the  soft  state  of  the 
skin  and  muscles. 

In  one  recent  case  I  hesitated  to  give  a  favourable 
prognosis,  as  the  symptoms  were  so  severe  and  the 
constitutional  disturbance  so  great.  The  patient  was 
a  boy,  12  years  of  age,  with  a  history  of  rheumatic 
fever.  His  condition  came  on  while  in  a  hospital,  and 
it  was  difficult  to  find  fault  with  the  diagnosis  of  rheuma- 
toid arthritis,  because  the  deformity  of  the  hands  was 
so  great.  There  was  abduction  of  the  hand,  with 
backward  displacement  of  several  finger-joints.  The 
knee?  were  in  a  condition  of  extreme  flexion,  and  both 
elbows  and  shoulders  had  very  limited  movements. 
But  there  was  an  absence  of  the  symptoms  which  I 
regard  as  essential  to  the  condition  to  which  I  think 
the  term  rheumatoid  arthritis  should  be  restricted  and 
which  I  shall  presently  describe. 

This  boy  had  pyretic  treatment  on  six  days  a  week 
for  nine  weeks.  During  the  whole  treatment  his  skin 
reaction  remained  persistently  very  acid,  only  showing 
a  diminution  during  the  last  week.  During  this  time 
he  gained  nearly  a  stone  in  weight.  His  general  health 
became  good,  and  gradually  the  joints  were  brought 


162  ARTHRITIS 

to  the  straight  position  without  any  forcible  breaking 
down  of  the  joints.  The  methods  used  were  those  I 
have  described.  In  this  case  the  boy  was  only  able 
to  walk  on  crutches  by  the  aid  of  splints  to  his  knees, 
when  dismissed  from  the  hospital.  When  once  this 
stage  is  reached  complete  recovery  is  only  a  matter  of 
time  and  exercise. 

RHEUMATOID    ARTHRITIS. 

This  name  can  be  properly  applied  to  a  disease  which 
is  readily  distinguishable  from  chronic  rheumatism.  If 
we  start  with  the  joint  symptoms,  it  will  be  found  that 
there  is  always  effusion  of  lymph,  not  only  extra- 
articular,  but  also  into  the  tissues  round  the  joint.. 
This  gives  the  peculiar  fusiform  appearance  to  the 
finger- joints  which  is  frequently,  but  not  by  any  means 
invariably,  found.  This  condition  does  not  occur  in 
chronic  rheumatism.  In  both  diseases  there  is  wasting 
of  muscle,  but  while  that  of  rheumatoid  arthritis 
precedes  the  joint  trouble,  that  of  chronic  rheumatism 
is  secondary  to  it,  and  partly  consequent  upon  it. 

But  the  most  marked  diagnostic  sign  is  the  condition 
of  the  muscle  itself.  In  rheumatoid  arthritis  it  is  soft, 
in  chronic  rheumatism  it  is  firm  and  resilient.  So 
marked  is  this  symptom,  and  so  generally  are  the  muscles 
affected,  that  even  in  a  case  where  the  ankle-joint  is 
alone  affected,  the  diagnosis  may  be  made  by  shaking 
hands  with  the  patient.  The  hand  of  the  patient  has 
a  soft  jelly-like  feel,  and  the  bones  are  distinguishable 
because  there  is  no  resiliency  in  the  muscles.  In  a 
large  number  of  cases  diagnosed  as  rheumatoid  arthritis 
it  is  only  necessary  to  shake  hands  with  the  patient, 
without  any  examination  of  the  joints  affected,  to  know 
that  the  diagnosis  is  wrong. 


RHEUMATOID   ARTHRITIS  163 

In  rheumatoid  arthritis  we  are  dealing  with  a  con- 
stitutional disease,  and  the  joint  symptoms  are  only  a 
symptom  of  the  condition.  The  patient  with  chronic 
rheumatism  may  be  a  person  of  sound  constitution 
and  robust  health  ;  the  rheumatoid-arthritis  patient 
is  always  debilitated. 

The  only  disorders  with  which  rheumatoid  arthritis, 
in  its  early  stages,  can  be  mistaken  for,  is  subacute 
articular  rheumatism  or  chronic  rheumatism  secondary 
to  rheumatic  fever.  Under  certain  conditions  the 
latter  cases  may  drift  into  those  of  true  arthritis. 
Given  an  anemic  girl  of  the  lactic-acid  diathesis,  and 
place  her  under  conditions  of  great  nervous  and  physi- 
cal strain,  or  subject  her  to  the  shock  of  operations, 
destructive  changes  may  take  place  in  the  joints  and 
the  condition  of  true  arthritis  may  develop. 

In  subacute  articular  rheumatism  we  may  have 
great  swelling  and  pain  in  the  joints,  but  no  destructive 
change  takes  place.  In  rheumatoid  arthritis  the 
erosion  of  the  synovial  membrane  commences  at  an 
early  stage,  and  the  whole  tissues  of  the  joint  gradually 
become  destroyed.  The  only  product  existing  in  the 
body  which  can  destroy  the  tissues  is  lactic  acid,  and 
the  patient  with  rheumatoid  arthritis  has  a  very  acid 
cutaneous  excretion.  But  this  is  also  true  of  the 
patient  with  subacute  rheumatism. 

We  know  that  if  we  place  some  meat  or  a  small  fish 
in  a  strong  solution  of  lactic  acid,  the  tissues  become 
friable  owing  to  the  complete  solution  of  the  phosphate 
of  lime.  The  lactic  acid  in  the  joint  of  the  patient 
with  rheumatoid  arthritis  has  not  that  greater  intensity 
which  would  explain  the  destruction  of  tissue.  We 
know,  however,  that  when  lactic  acid  invades  the  cell- 
wall  it  is  the  phosphate  of  lime  which  neutralizes  it 


164  ARTHRITIS 

and  holds  it,  so  that  it  cannot  invade  the  protoplasm  of 
the  cell.  We  know  that  in  the  healthy  cell  the  invasion 
of  an  extra  quantity  of  lactic  acid  has  the  the  effect  of 
causing  stiffness  of  the  tissues,  with  greater  rigidity,  such 
as  we  find  in  chronic  rheumatism.  But  this  is  due  to  its 
combination  with  phosphate  of  lime  in  the  cell-wall. 

If  we  suppose  that  there  is  a  great  diminution  in  the 
normal  amount  of  phosphate  of  lime  in  the  cell- wall, 
it  would  account  for  the  want  of  tone  and  resiliency 
in  the  muscle,  and  it  would  also  account  for  the  fact 
that  the  tissues  of  the  joint  when  invaded  by  lactic 
acid  are  unable  to  neutralize  it  or  prevent  its  action 
upon  the  protoplasm  of  the  cells.  This  being  so,  we 
shall  not  require  a  higher  degree  of  acidity  than  that 
which  exists  in  ordinary  rheumatism  to  produce  the 
destructive  changes  in  the  joints.  These  facts  led  me 
to  take  the  view  that  the  constitutional  condition  which 
causes  rheumatoid  arthritis  is  one  in  which  the  power 
to  assimilate  the  lime  salts  is  deficient,  or  the  supply 
of  lime  is  insufficient,  and  that  it  is  when  this  condition 
is  coupled  with  the  lactic-acid  diathesis  that  we  have 
the  joint  conditions  peculiar  to  the  disease. 

Just  as  I  found  that  people  living  in  districts  where 
the  drinking  water  was  very  hard  and  contained 
carbonate  of  lime  had  a  greater  tendency  to  lithic 
deposits  than  others,  so  I  have  found  that  in  certain 
districts  where  the  water  is  soft  and  free  from  lime 
true  rheumatoid  arthritis  occurs  more  frequently.  My 
observations  on  this  point  have  not  been  sufficient  to 
enable  me  to  speak  positively,  but  I  think  it  is  one 
well  worthy  of  further  inquiry,  and  also  as  to  whether 
there  are  not  other  sources  of  deficiency  of  lime  in  the 
dietary. 

The    importance    of    providing    sufficient    mineral 


RHEUMATOID  ARTHRITIS  165 

matter  to  feed  the  cell-wall  is  evident,  and  there  is  an 
agricultural  problem  which  points  to  the  same  fact. 
It  is  found  that  if  the  soil  is  made  rich  in  nitrogenous 
matter  by  fertilizers,  it  is  possible  to  grow  corn  with 
large  heads  and  heavy  with  grain  ;  but  when  this  is  done 
the  stalk  does  not  support  the  head,  which  falls  to  the 
ground,  and  therefore  the  result  is  not  satisfactory. 
Now  straw  contains  a  large  amount  of  lime  in  the  cell- 
walls,  and  it  is  evident  that  a  crop  of  corn  makes  a 
great  drain  upon  the  available  lime  in  the  soil. 

On  theoretical  grounds  I  should  suggest  that  the 
difficulty  would  be  surmounted  if,  instead  of  relying 
wholly  upon  nitrogenous  fertilizers,  lime  was  regularly 
added  to  the  soil  where  corn  is  grown.  I  have  no 
knowledge  of  agricultural  chemistry,  but  I  think  that 
both  in  medicine  and  agriculture  the  importance  of  lime 
as  a  necessary  food  should  be  recognized. 

In  'rheumatoid  arthritis ',  and  in  all  cases  where  I 
have  found  great  loss  of  resiliency  in  the  muscles,  I  have 
found  a  solution  of  the  phosphate  of  lime  in  phosphoric 
acid  give  remarkable  results :  so  much  so  that  I  think 
it  is  the  absence  of  lime  from  the  diet,  rather  than 
the  loss  of  power  to  assimilate  it,  which  is  the  cause 
of  the  conditions  found  in  this  disease.  The  rapid  pulse 
and  the  relaxed  condition  of  the  blood-vessels  also 
become  more  normal  when  this  remedy  is  given.  I 
found  that  a  more  soluble  phosphate  of  lime  could 
be  produced  by  the  addition  of  a  small  quantity  of 
the  perchloride  of  iron.  The  following  is  the  formula 
I  employ  : — 

R   Calc.   Phos.  gr.  cxcij       Acid.  Phos.   Cone.         5  xivss 

Liq.  Ferri  Perchlor.    Dil.  3'j       Aq.  ad  giv 

Of  this,  ten  drops  are  given  in  water  thrice  daily  before 
meals. 


166  ARTHRITIS 

It  will  be  understood  that  I  use  this  preparation  in 
cases  of  true  rheumatoid  arthritis,  because  it  is  indicated 
by  the  symptoms  present.  It  would  do  more  harm  than 
good  if  prescribed  for  cases  which  have  received  the 
name  of  rheumatoid  arthritis  but  have  none  of  the 
symptoms  which  I  have  described  as  characteristic  of 
the  disease. 

It  is  of  very  great  importance  to  remove  the  excess 
of  lactic  acid  from  the  tissues  by  pyretic  treatment.  As 
this  involves  raising  the  body  temperature  and  causing 
free  sweating,  some  physicians  have  thought  that  it 
would  have  a  debilitating  effect  upon  a  patient  already 
weak,  and  whose  heart  is  rapid.  As  a  matter  of  fact, 
when  the  treatment  is  properly  conducted,  the  patients 
improve  in  weight,  and  the  irritable  heart  due  to  the 
excess  of  free  acid  becomes  rapidly  improved. 

The  prognosis  of  any  case  of  rheumatoid  arthritis 
depends. upon  the  degree  of  destructive  changes  which 
have  already  taken  place  ^n  the  joints.  Further  destruc- 
tive changes  are  arrested  when  efficient  treatment  is 
given  ;  the  difficulty  is  to  repair  the  damage  already 
done. 

Formerly  I  regarded  it  as  impossible  to  obtain  renewal 
of  the  tissues  and  cartilages  of  the  joint  when  once 
destroyed  ;  but  I  have  seen  so  many  cases  where  repair 
has  taken  place  and  a  useful  joint  has  resulted,  that  I 
think  it  well  worth  while  to  give  time  and  trouble  to 
securing  this  end  ;  this  is  most  difficult,  but  also  most 
necessary,  in  the  case  of  the  knee-joint. 

There  is  a  physical  point  of  importance  in  these  cases. 
Under  all  circumstances  where  there  is  heat  in  a  joint 
absolute  rest  is  indicated  ;  but  in  these  cases  where 
there  is  slight  heat — and  it  is  seldom  very  great — it  is 
necessary  to  give  some  passive  movements  every  day, 


RHEUMATOID   ARTHRITIS  167 

otherwise  there  is  a  danger  of  ankylosis.  But  in  a 
joint  such  as  the  knee,  the  weight  of  the  body  should 
not  be  allowed  to  be  put  upon  the  joint,  and  it  is  often 
necessary  to  use  a  splint  which  prevents  eversion  of  the 
foot.  In  such  cases,  a  continuous  compress  (moist),  a 
proper  splint,  and  daily  passive  movements,  give  slow 
but  satisfactory  results. 

In  many  cases,  if  the  joint  is  flexed  to  its  fullest 
extent,  fluid  will  be  found  ;  and  this  must  be  removed 
by  a  blister  as  a  preliminary  to  all  other  treatment, 
lonization  is  a  very  inefficient  remedy  for  this  condition. 
In  cases  where  there  is  neither  heat  nor  fluid  in  the 
joint,  rest  of  the  joint  so  far  as  the  weight  of  the  body 
is  concerned  is  imperative  in  the  early  stage,  but  passive 
movements  must  be  given  daily.  A  splint  is  only 
indicated  if  there  is  a  tendency  to  deformity.  As  the 
patient  improves,  resisted  movements  may  be  given 
with  advantage. 

In  many  advanced  cases  of  rheumatoid  arthritis  that 
come  under  my  notice,  I  find  that  the  actual  progress 
of  the  disease  has  been  for  some  time  arrested.  The 
joints  which  retain  a  measure  of  mobility  are  those 
which  the  patient  has  been  obliged  to  use.  It  is  for 
this  reason  that  from  the  first  indication  of  the  disease 
the  patient  should  be  encouraged  to  put  every  joint 
in  the  body  through  its  full  movements  daily.  Nothing 
favours  ankylosis  of  the  joints  in  such  cases  more  than 
the  absence  of  their  normal  physiological  activity. 
This  does  not  mean  that  the  patient  should  be  taught 
to  walk  on  an  inflamed  or  impaired  joint,  or  strain  the 
parts  which  enter  into  their  mechanism.  Exercise 
must  be  slow  and  gentle,  and  is  most  valuable  when  it 
is  the  result  of  the  patient's  personal  effort. 

I  have  mentioned  the  debilitated  form  of  chronic 


168  ARTHRITIS 

rheumatism  which  sometimes  follows  rheumatic  fever. 
In  these  cases  the  solution  of  phosphate  of  lime  is  a 
very  valuable  remedy,  as  it  is  in  others  with  no 
arthritic  tendency  but  with  a  debilitated  state  of 
the  tissues  and  loss  of  resiliency  in  the  muscles. 

It  is  intelligible  that  when  the  cell-wall  is  so  deficient 
in  lime  that  it  cannot  resist  the  normal  acids  of  the 
body,  it  may  also  lack  resistance  to  micro-organisms. 
Therefore,  if  a  patient  exhibiting  the  symptoms  of 
rheumatoid  arthritis  has  any  condition  causing  auto- 
infection,  such  as  pyorrhoea  or  any  other  discharge, 
the  bacilli  may  add  to  the  mischief  in  the  joints  and 
make  the  treatment  less  efficient.  Hence  in  these 
cases  it  is  not  unreasonable  to  look  for  such  possible 
causes  of  infection  and  remove  them  if  we  can.  But 
if  the  view  is  taken  that  these  conditions  are  the  cause 
of  the  disease  and  their  removal  is  a  sufficient  treat- 
ment, the  results  will  always  be  unsatisfactory,  and 
grave  harm  will  be  done  by  the  delay  of  treatment 
which  in  these  cases  is  urgently  required.  In  true  cases 
of  rheumatoid  arthritis  the  destructive  changes  in  the 
joints  take  place  very  rapidly,  and  the  removal  of  the 
excess  of  acid  and  the  proper  nutrition  of  the  cell-walls 
demands  the  first  attention.  It  does  not  follow  that 
even  if  a  source  of  infection  is  discovered  it  is  of 
necessity  a  cause  of  injury  to  the  joints.  Some  means 
should  be  taken  to  ascertain  this  point  before  operative 
measures  or  vaccines  are  prescribed.  I  will  explain 
the  method  I  adopt  in  the  course  of  this  chapter. 

In  true  chronic  rheumatism  I  have  never  seen  the 
course  of  the  disorder  influenced  by  the  existence,  or 
removal,  of  sources  of  infection,  or  by  vaccines  ;  I  have 
only  seen  great  harm  done  by  the  delay  of  necessary 
treatment.  I  believe  in  these  cases  the  cell-wall  is 


169 

proof  against  infection  by  bacilli.  But  in  the  debility 
and  arthritic  conditions  following  rheumatic  fever,  and 
in  true  rheumatoid  arthritis,  I  think  the  possible 
influence  of  bacilli  is  a  factor  which  may  have  to  be 
dealt  with. 

Cases  of  subacute  rheumatism  in  anaemic  girls  make 
rapid  improvement  when  pyretic  treatment  is  given  ; 
but  if  diagnosed  as  rheumatoid  arthritis  and  treated 
with  vaccines  the  results  may  be  disastrous. 

I  was  consulted  about  one  case,  a  rather  delicate  girl 
of  18,  who  had  an  attack  of  subacute  rheumatism.  Her 
parents  regarded  her  as  too  weak  to  undergo  pyretic 
treatment,  and  sent  her  to  London.  Her  case  was 
diagnosed  as  rheumatoid  arthritis,  and  her  tonsils  were 
removed  and  a  course  of  vaccine  given.  No  improve- 
ment took  place.  It  was  then  decided  that  the  remains 
of  the  tonsils  must  be  enucleated.  This  was  done,  and 
more  vaccine  was  given.  As  she  did  not  improve,  her 
uterus  was  curetted  !  When  I  last  heard  of  her  she  was 
a  physical  wreck,  confined  to  her  bed,  and  her  condition 
was  attributed  to  rheumatoid  arthritis  ! 

CHRONIC     LITHITIS     OR     GOUT. 

The  symptoms  presented  by  a  case  of  chronic  lithitis 
or  gout  are  so  opposite  to  those  met  with  in  rheumatoid 
arthritis,  that  it  is  difficult  to  understand  how  any 
confusion  can  exist  between  the  two  disorders.  The 
typical  patient  with  the  chronic  and  subacute  forms 
of  multi-articular  gout  has  a  sound  constitution  and 
good  family  history.  The  muscles  are  firm  and  there 
is  no  tendency  to  wasting  of  muscles,  except  any  which 
may  be  due  to  loss  of  physical  activity  owing  to  a  joint 
becoming  incapable  of  use.  The  hair  is  frequently 
prematurely  grey,  the  skin  may  be  inactive,  and  the 


170  ARTHRITIS 

temperature  below  normal ;  but  this  does  not  affect  the 
muscular  activity  of  the  patient. 

As  I  have  previously  pointed  out,  the  presence  of 
lithates,  either  intra-  or  extra-articular,  is  not  of  neces- 
sity accompanied  by  pain  ;  but  attention  is  usually 
called  to  the  disorder  either  because  one  or  more  joints 
have  become  painful,  or  actual  swelling  of  the  small 
joints  of  the  hand  is  noticed.  This  swelling  is  hard 
and  nodular  (except  in  the  acute  form),  and  is  due  to 
the  deposit  of  lithates  external  to  the  joint  and  with 
or  without  some  enlargement  of  the  heads  of  the 
phalanges.  There  is  an  excess  of  phosphate  of  lime  in 
the  tissues  instead  of  the  insufficiency  found  in  rheuma- 
toid arthritis.  To  suggest  that  a  case  of  this  kind  is  due 
to  the  action  of  bacilli,  and  to  order  teeth  to  be  extracted, 
and  place  the  patient  upon  vaccine  treatment,  is  an 
error  which  no  practitioner  should  make.  The  sym- 
ptoms we  meet  with  are  invariably  due  to  the  efforts 
of  the  organism  to  free  itself  from  the  lithates.  These 
efforts  may  be  inefficient,  and  put  the  patient  to  much 
pain  and  trouble ;  but  the  business  of  the  physician  is 
to  assist  the  natural  process  of  recovery,  not  to  try  and 
check  it. 

The  acute  attack  gives  us  the  indications  for  the  line 
of  treatment  which  may  be  used  in  the  more  chronic 
forms  with  success.  In  acute  gout  we  have  a  rise  of 
temperature,  during  which  the  patient  may  break  into 
a  sweat  which  is  very  acid  over  the  joints  affected.  A 
process  takes  place  by  which  there  is  effusion  into  the 
tissues  around  the  lithate  which  tends  to  dissolve  it, 
and  at  the  same  time  there  is  liberation  of  lactic  acid, 
as  the  examination  over  the  affected  joints  shows. 

Xow  we  can  reproduce  these  phenomena  in  chronic 
cases  by  pyretic  treatment,  and  we  can  cause  effusion 


CHRONIC   LITHITIS   OR   GOUT  171 

into  the  tissues  round  the  lithate  by  continued  electric 
vibration.  For  this  purpose  it  is  necessary  to  use  a 
vibrator  which  rotates  like  a  drill,  except  when  it  is 
placed  in  contact  with  the  skin,  and  not  one  in  which 
the  vibration  depends  upon  the  movement  of  an  ex- 
centric  wheel.  The  effect  of  the  former  is  to  raise  the 
temperature  of  the  tissues  to  which  it  is  applied,  pro- 
viding it  is  used  at  the  required  point  for  seven  to  ten 
minutes.  The  use  of  this  appliance  is  contra-indicated 
in  cases  where  there  is  any  heat  on  the  surface  of  the 
joint  because,  in  such  cases,  it  would  set  up  too  much 
effusion  in  the  joint  and  produce  an  acute  attack,  which 
is  undesirable.  Like  all  treatments  for  joint  cases,  it 
requires  steady  perseverance  to  remove  the  lithates 
from  the  tissues.  The  immediate  effect  is  often  remark- 
able, because  a  joint  stiffened  and  painful  to  move 
becomes  readily  movable  and  painless  after  a  single 
vibration.  This  is  due  to  the  fluid  effused  into  the 
tissues.  As  this  is  absorbed,  the  stiffness  returns, 
but  each  time  some  solution  of  the  lithates  takes  place, 
so  that  finally  they  are  disposed  of. 

In  the  acute  cases  where  this  treatment  would  be 
contra-indicated,  the  application  of  a  strong  solution  of 
salicylate  of  soda,  well  rubbed  into  the  skin,  followed 
immediately  by  the  liniment  of  iodine  or  the  tincture, 
applied  as  a  paint,  is  very  useful.  The  chemical  action 
taking  place  in  the  skin  produces  results  which  would 
not  be  obtained  by  mixing  the  two  solutions  before 
they  were  applied. 

I  have  described  the  conditions  under  which  the 
lithates  are  formed  in  the  tissues,  and  also  the  processes 
which  take  place  when  the  lithates  undergo  decomposi- 
tion, and  the  symptoms  produced.  I  have  already 
suggested  that  when  we  find  lithates  in  or  around  a 


172  ARTHRITIS 

joint  causing  no  pain  other  than  any  which  may  be 
produced  by  their  mechanical  presence,  we  should 
describe  it  as  a  lithic  joint  and  the  patient  as  having 
the  lithic  diatheses.  When  there  is  pain  owing  to  the 
lithates  undergoing  decomposition,  we  may  speak  of 
it  as  acute  or  subacute  lithitis.  I  think  the  word 
'  gout ',  expressing  as  it  does  a  wrong  idea  of  the 
cause  and  nature  of  the  disorder,  is  undesirable.  I 
regret  that  I  have  been  compelled  to  use  it  in  the 
title  of  this  work. 

There  are  other  symptoms  connected  with  subacute 
lithitis  which  will  be  best  described  in  the  chapter  on 
'neuritis'. 

RHEUMATIC    GOUT. 

This  name,  although  it  has  gone  out  of  use,  does  well 
enough  to  describe  a  form  of  chronic  joint  trouble 
frequently  met  with.  In  this  disorder  there  is  a  good 
deal  of  thickening  of  the  tissue  immediately  round  the 
joints.  This  is  solid,  and  not  fluctuating  as  in  rheu- 
matoid arthritis.  It  covers  a  larger  area,  and  is  more 
irregular  than  the  enlargement  of  the  small  joints  of 
the  hand  which  we  find  in  chronic  gout  or  patients 
with  the  lithic  diathesis,  who  may  never  have  any 
symptoms  of  gout  in  spite  of  the  lithates  round  the 
joints. 

Some  writers  have  doubted  the  co-existence  of 
rheumatism  and  gout.  It  does  not  appear  probable 
that  the  two  disorders  would  exist  in  the  same  person, 
because  a  deficiency  of  lactic  acid  leads  to  the  deposit 
of  lithates,  while  rheumatism  is  due  to  an  excess  of  the 
acid.  But  clinically  we  meet  with  cases  where  minute 
lithates  which  have  existed  in  the  tissues  surrounding 
a  joint  have  become  involved  in  an  acute  or  subacute 


RHEUMATIC   GOUT  173 

attack  of  rheumatism,  and  as  a  result  the  swelling  of 
the  joints  characteristic  of  rheumatic  gout  has  been 
produced.  For  some  reason  which  I  do  not  clearly 
understand,  this  may  happen  at  the  end  of  an  attack 
of  acute  rheumatism  when  all  the  typical  rheumatic 
symptoms  in  the  joint  have  subsided.  More  usually 
it  occurs  at  an  early  stage.  The  following  case  is  very 
instructive  in  this  connection  : — 

A  physician  in  the  South  of  England  wrote  to  me 
about  a  young  lady  who  had  a  number  of  swollen  joints. 
He  took  her  to  a  great  specialist,  who  pronounced  the 
case  one  of  rheumatoid  arthritis,  and  gave  the  opinion 
that  she  would  be  crippled  in  every  joint  within  two 
years.  Soon  after,  sugar  was  found  in  the  urine  of  the 
patient,  and  she  was  taken  to  another  specialist,  who 
took  a  very  grave  view  and  thought  that  she  would  not 
live  two  years.  But  the  physician  had  been  treating 
her  with  iodide  of  iron,  and  instead  of  growing  worse 
she  appeared  to  improve ;  he  therefore  asked  me  to 
see  if  anything  further  could  be  done  for  her.  On 
shaking  hands  with  the  patient,  a  healthy-looking  girl, 
she  gave  me  a  firm  grip  which  at  once  dissipated 
the  idea  of  rheumatoid  arthritis.  On  triturating  the 
tissues  with  the  finger  over  the  affected  joints  I  could 
clearly  make  out  a  number  of  tiny  particles  like  firm 
sand  in  the  tissues.  I  formed  the  opinion  that  she  was 
suffering  from  subacute  rheumatism,  and  that  the 
action  of  the  lactic  acid  upon  these  minute  lithates 
accounted  for  the  appearance  presented  by  the  joints  ; 
a  subacute  lithitis  had  been  set  up.  I  gave  her  pyretic 
treatment  for  one  month,  and  at  the  end  of  this  time 
she  was  quite  well,  both  as  regards  the  joints  and  the 
glycosuria.  I  suggested  a  further  course  of  treatment 
in  six  months,  but  at  the  end  of  that  time  she  remained 


174  ARTHRITIS 

so  well  that  it  did  not  appear  necessary.  The  formation 
of  lithates  and  the  existence  of  glycosuria  both  pointed 
to  '  gout ',  but  the  joint  symptoms  were  '  rheumatic  '. 

Rheumatic  gout  must  be  regarded  as  a  very  distinct 
disorder,  and  is  an  attack  of  rheumatism  in  a  patient 
who  has  lithates  already  deposited  in  or  around  the 
joints.  As  I  have  shown,  a  person  may  have  lithates 
in  various  tissues  for  many  years  and  never  have  an 
attack  of  rheumatism  or  gout.  The  attack  of  gout  is 
most  likely  to  occur  when  there  are  concretions  of 
lithates  in  a  joint,  and  it  occurs  usually  in  one  or  two 
joints  as  a  local  affection  due  to  the  condition  of  the 
tissues  immediately  surrounding  the  concretion,  so  that 
other  joints  in  which  lithates  exist  are  not  attacked. 

But  when  a  patient  with  lithates  in  the  joints  is 
attacked  by  rheumatism,  it  is  due  to  the  circulation 
of  free  lactic  acid,  and  therefore  a  large  number  of 
joints  are  attacked  simultaneously,  and  in  many  of 
these  joints  the  lithates  may  be  so  small  and  scattered 
in  the  tissues  that  it  is  difficult  to  detect  their  presence. 
The  skin  of  the  patients  when  so  attacked  has  the 
acid  reaction  and  the  soft  adhesive  feeling  of  the  rheu- 
matic patient,  while  that  of  the  gouty  patient  is  very 
slightly  acid  in  reaction  and  only  gradually  increases 
in  acidity,  and  the  skin  is  brought  into  action  and 
lactic  acid  liberated  from  the  tissues  by  treatment. 

While  during  the  period  when  the  lithates  are  deposited 
in  the  joints  the  patient  may  have  a  deficiency  of  lactic 
acid,  there  is  no  physiological  reason  to  prevent  the 
same  patient  manufacturing  an  excess  of  lactic  acid 
under  changed  conditions.  In  fact  this  does  occur 
normally  when  the  patient  takes  vigorous  and  un- 
accustomed exercise ;  but  the  usual  result  is  simply  to 
dissolve  the  lithates  without  the  production  of  pain  or 


RHEUMATIC   GOUT  175 

discomfort.  It  is  only  when  the  tissues  have  become 
saturated  with  lactic  acid  that  a  true  rheumatic  attack 
is  produced,  and  then  the  presence  of  the  lithates 
influences  the  attack  and  alters  the  appearance  of  the 
joints. 

The  treatment  of  rheumatic  gout  is  the  same  as  for 
rheumatism  either  in  its  acute  or  chronic  form.  When 
we  have  removed  the  excess  of  lactic  acid  from  the 
tissues,  the  attack  ceases,  whether  all  the  lithates  have 
been  removed  or  not. 

There  is  another  class  of  case  closely  allied  to  rheu- 
matic gout  in  which,  instead  of  a  firm  swelling  of  the 
joints,  the  condition  is  one  where  there  may  be  little 
actual  enlargement,  but  the  tissues  around  the  joint 
have  a  puffy  appearance  which  gives  the  appearance 
of  considerable  swelling.  These  cases  have  some 
resemblance  to  a  joint  swollen  from  the  effect  of  myx- 
cedema.  There  is  swelling  without  effusion  of  lymph, 
but  the  form  is  less  regular. 

The  actual  joint  symptoms  may  be  those  of  chronic 
rheumatism  or  rheumatic  gout  ;  but  these  cases  have 
less  tendency  to  clear  up  with  the  same  treatment, 
although  they  derive  benefit,  the  pain  being  relieved 
and  the  movements  of  the  joints  improved. 

I  formed  the  conclusion  many  years  ago  that  these 
cases  were  complicated  by  the  existence  of  micro- 
organisms in  the  tissues,  probably  what  we  now 
recognize  as  streptococci  and  staphylococci.  I  did  not 
reach  this  conclusion  as  a  result  of  bacteriological 
examination,  because  it  was  before  the  bacteriological 
theory  of  rheumatism  was  introduced,  I  formed  the  view 
from  clinical  experience. 

To  trace  the  history  of  such  cases  we  have  to  go 
back  to  the  early  life  of  the  patient.  We  can  usually 


176  ARTHRITIS 

obtain  information  of  some  skin  disease  or  the  sudden 
suppression  of  an  eruption.  We  next  may  get  a 
history  of  some  ailments  other  than  the  joint  trouble, 
which  may  only  appear  at  a  later  stage  in  life.  One  of 
these  ailments  is  a  headache,  recurring  at  regular 
intervals — it  may  be  one  day  in  the  week  or  fortnight — 
and  this  condition  may  persist  for  many  years.  About 
the  age  of  45  or  50  the  headaches  may  cease,  and  the 
patient  may  develop  the  form  of  joint  disease  I  am  now 
describing.  But  I  have  known  these  headaches  con- 
tinue to  the  age  of  68  and  grow  worse.  I  cured  one 
such  patient  in  whom  the  attacks  had  existed  since  she 
was  9  years  of  age. 

The  appearance  of  joint  symptoms  is  by  no  means 
an  invariable  result  of  this  disorder.  Such  symptoms 
only  occur  in  those  who  have  the  lithic  or  lactic-acid 
diathesis,  and  who  would  have  developed  joint  sym- 
ptoms in  any  case,  but  not  in  the  same  form. 

I  have  never  taken  the  view,  nor  do  I  now  in  spite  of 
all  that  has  been  written,  that  any  micro-organisms  can 
cause  joint  disease  ;  but  I  am  equally  strongly  convinced 
that  they  can  alter  the  character,  increase  the  severity, 
and  prolong  the  duration.  It  is  just  as  likely  that  the 
conditions  I  have  mentioned  will  cause  an  intractable 
form  of  asthma,  and  that  this  may  occur  in  patients 
with  lactic-acid  diathesis,  who  might  be  expected  to 
develop  joint  troubles. 

Since  writing  the  last  paragraph  I  have  seen  a  lady 
who  suffered  from  these  recurrent  headaches  during 
the  whole  of  her  early  life.  In  1903  she  was  vaccinated 
during  a  small-pox  scare.  Inflammation  occurred  at 
the  site  of  vaccination  and  spread  to  the  whole  arm, 
and  for  nine  months  she  had  a  series  of  'abscesses'  and 
eruptions  in  all  parts  of  the  body.  Her  condition  was 


RHEUMATIC    GOUT  177 

diagnosed  as  blood-poisoning  ;  but  in  spite  of  all  her 
sufferings  her  health  was  better  than  it  had  been  for 
years,  and  the  headaches  entirely  ceased.  I  take  the 
view  that  the  bacilli  which  caused  all  the  trouble  were 
not  introduced  from  without,  but  that  the  vaccination 
set  up  an  effort  of  the  organism  to  throw  out  the  bacilli 
which  had  existed  in  the  tissues  since  early  life,  and 
had  caused  the  symptoms  from  which  she  suffered. 
I  have  ample  grounds  for  this  belief  on  the  evidence 
of  clinical  experience.  I  mentioned  that  I  cured  a 
lady  of  these  recurrent  headaches  at  the  age  of  68.  I 
did  so  by  artificially  producing  eruptions  over  the 
abdomen  and  in  various  parts  of  the  body,  and  repeating 
the  treatment  for  many  weeks.  I  have  done  the  same 
in  a  very  large  number  of  cases,  with  invariable  success. 

My  attention  was  first  called  to  the  connection  of 
this  condition  with  asthjna  by  the  following  case  :  — 

A  lady,  who  was  a  chronic  asthmatic,  had  some  pain 
in.  the  region  of  the  hip,  and  rubbed  in  a  well-known 
embrocation,  as  a  remedy.  The  result  was  a  large 
inflammatory  area  over  the  site  of  the  application, 
closely  resembling  erysipelas.  This  spread  down  the 
whole  limb  and  subsequently  invaded  the  opposite 
side.  She  had  a  good  deal  of  pain  and  suffering,  which 
lasted  for  nearly  three  weeks.  At  the  end  of  this  time 
the  skin  was  healed  and  the  asthma  had  quite  dis- 
appeared. She  lived  for  many  years  after  this,  and  the 
chronic  asthma  remained  entirely  cured. 

This  experience  induced  me  to  try  the  effect  of  an 
artificial  eruption  in  other  cases.  I  found  that  in  cases 
suitable  for  this  treatment — that  is  to  say,  those  who 
had  staphylococci  in  their  tissues — a  few  days  after 
rubbing  the  skin  with  a  liniment  composed  of  lini- 
mentum  crotonis  and  linimentum  saponis,  equal  parts, 


178  ARTHRITIS 

a  pustular  eruption  developed.  In  some  cases  the 
application  only  set  up  a  dermatitis,  and  I  did  not 
persevere  in  those  cases.  But  when  the  pustular  erup- 
tion was  produced,  I  maintained  it  by  mild  applications 
from  time  to  time  so  long  as  it  could  be  made  to  persist. 
Long-continued  treatment  was  necessary  to  obtain 
permanent  results.  The  following  case  has  many 
instructive  features  : — 

A  boy  at  the  age  of  5  had  measles  ;  it  was  followed 
by  asthma,  which  continued  until  the  time  of  admission 
to  hospital  when  he  had  reached  the  age  of  16.  He 
was  much  stunted  in  growth,  and  weighed  only  4  st.  7  Ib. 
The  attacks  during  the  previous  three  years  had  greatly 
increased  in  severity,  with  continual  cough  between 
the  attacks.  During  the  attacks  there  was  great 
dyspnoea,  violent  coughing  with  expectoration,  and 
profuse  perspiration.  The  liniment  I  have  mentioned 
was  applied  to  the  whole  of  the  front  of  the  chest  and 
abdomen,  and  produced  a  crop  of  pustules  over  the 
entire  surface.  This  was  maintained  for  eight  weeks. 
During  this  time  the  temperature  was  artificially  raised 
about  3°  each  day,  and  profuse  sweating  produced. 
The  reaction  of  the  cutaneous  excretion  was  intensely 
acid,  and  remained  so  until  the  twenty-eighth  applica- 
tion of  the  process  ;  it  then  diminished  until  the  fortieth 
administration,  when  the  boy  had  a  slight  cold  and 
the  reaction  became  excessively  acid  and  remained  so 
for  six  days  ;  it  then  fell  to  normal. 

This  case  shows  that  the  boy  had  a  very  marked 
lactic-acid  diathesis,  and  also  the  large  number  of 
baths  which  are  necessary  to  clear  the  tissues  of  the 
accumulated  acid.  As  the  boy  was  in  a  debilitated 
state  on  admission,  those  unaccustomed  to  the  treatment 
would  think  that  eight  weeks  of  daily  baths,  each 


RHEUMATIC   GOUT  179 

causing  a  rise  of  temperature  and  profuse  sweating, 
would  have  increased  the  debility.  His  condition  at 
the  end  of  this  period  was  as  follows.  The  attacks  of 
asthma,  which  had  been  milder  and  less  frequent  during 
the  early  stages  of  treatment,  had  disappeared  for  a 
fortnight.  The  boy  looked  perfectly  well  and  expressed 
himself  as  feeling  well.  His  weight  was  5  st.  6i  lb., 
showing  a  gain  of  nearly  one  stone.  The  circumference 
of  the  chest  had  increased  by  four  inches. 

The  introduction  of  cases  of  asthma  into  a  chapter 
on  arthritis  may  appear  to  be  a  digression  ;  but,  in 
the  class  of  joint  disease  I  am  considering,  the  patho- 
logical conditions  appear  to  be  identical  so  far  as  the 
cause  of  the  disease  is  concerned.  When  we  meet  with 
such  cases — and  they  occur  with  some  frequency — it 
is  always  well  to  test  the  reaction  of  the  patient  to 
stimulating  liniments,  and  if  there  is  decided  irritability 
of  the  skin  we  can  be  sure  of  benefit  resulting  from 
their  persistent  application,  whether  over  the  affected 
joints  or  at  some  more  convenient  part  of  the  body. 
It  is  in  this  particular  class  of  case  that  vaccines  may 
be  expected  to  do  good.  They  may  accomplish  good 
because  they  antidote  the  cause  of  irritation  which 
maintains  and  increases  the  joint  trouble  and  leads  to 
its  indefinite  continuance ;  but  no  vaccine  can  remove 
the  excess  of  lactic  acid  from  the  tissues,  and  therefore 
it  can  only  effect  a  cure  when  it  excites  a  reaction 
resulting  in  a  continued  rise  of  temperature,  or,  in 
other  words,  induces  the  condition  which  nature  uses 
to  eliminate  the  acid. 

But  personally,  I  have  never  felt  justified  in  setting 
up  a  toxic  fever  when  one  can  accomplish  the  same 
result  by  physiological  methods,  and  at  the  same  time 
improve  the  health  of  the  patient,  which  a  toxic  fever 


180  ARTHRITIS 

never  does.  The  combination  of  mild  doses  of  vaccine 
with  pyretic  treatment  may  prove  an  efficient  method 
of  dealing  with  such  cases  ;  but  the  method  I  used 
before  the  bacteriological  theory  was  introduced  has 
given  such  good  results  that  perhaps  I  am  prejudiced 
in  its  favour. 

ARTHRITIS    DEFORMANS. 

There  is  another  form  of  joint  disease  for  which  the 
name  arthritis  deformans  appears  very  suitable.  In 
all  cases  where  destructive  changes  take  place  in  the 
joint  there  may  be  a  certain  amount  of  deformity — 
flexion,  abduction  of  the  hand,  or  backward  displace- 
ment of  the  finger- joints ;  but  in  this  disease  the 
deformity  is  the  most  marked  and  characteristic  feature, 
and  in  pure  cases  there  may  be  very  little  swelling 
of  the  joint,  no  tendency  to  the  lactic  acid  diathesis, 
and  an  absence  of  lithates.  As,  however,  this  disorder 
may  attack  persons  of  either  the  lithic  or  lactic-acid 
diathesis,  the  condition  is  sometimes  more  complicated. 

When  we  meet  with  this  condition  there  is  almost 
invariably  the  history  of  either  some  nervous  shock  or 
prolonged  nervous  strain  combined  with  physical 
exhaustion.  In  pure  cases,  the  destructive  changes  in 
the  joints  are  not  due  to  the  erosion  of  lactic  acid  as  in 
rheumatoid  arthritis,  but  to  an  asthenic  condition  of 
the  nerves  supplying  the  joint.  We  are  dealing  in  these 
cases  with  a  direct  disease  of  the  central  nervous 
system,  and  while  the  symptoms  may  simulate  those 
of  rheumatism  and  rheumatoid  arthritis,  the  pathology 
of  the  disorder  is  wholly  distinct.  The  only  source  of 
confusion  arises  from  the  fact  that  while  in  the  true  cases 
the  asthenic  condition  of  the  articular  nerves  is  of 
central  origin,  we  may  have  cases  of  joint  trouble 


ARTHRITIS   DEFORMANS  181 

where  an  asthenic  condition  of  certain  nerves  is  purely 
local,  and  only  affects  the  area  of  distribution  of  the 
particular  nerves  affected. 

To  illustrate  the  pathology  of  such  cases,  I  may 
mention  the  case  of  an  officer  of  Horse  Artillery.  He 
had  nothing  the  matter  with  his  joints,  but  he  had  on 
the  outside  of  the  left  knee-joint  a  small  area  of  skin 
which  had  shrivelled  and  become  entirely  numb.  The 
skin  had  a  blanched  appearance,  and  the  surface 
resembled  the  goose  skin  condition  which  follows  the 
application  of  intense  cold  to  the  skin.  The  trouble 
corresponded  exactly  with  the  area  of  distribution  of 
the  external  cutaneous  nerve.  I  found  this  nerve 
practically  paralyzed.  The  cause  was  obvious  :  when 
riding  over  difficult  country,  in  command  of  a  mountain 
battery,  the  hilt  of  his  sword  was  continually  per- 
cussing this  nerve  and  had  induced  the  condition. 
This  case  shows  that  injury  to  a  nerve-trunk  may  set 
up  trophic  changes  in  the  area  of  its  supply.  Thus 
atrophic  disease  of  the  hip-joint  is  due  to  definite  injury 
or  pressure  upon  a  branch  of  the  obturator  nerve  in 
the  pelvis,  as  I  shall  presently  mention. 

Another  case  well  illustrates  the  fact  that  a  local 
arthritis  deformans  can  be  produced  by  injury  to  the 
nerves.  A  lady,  while  travelling  abroad,  injured  her 
wrist ;  the  local  surgeon  consulted  said  that  it  was 
fractured,  and  kept  the  wrist  and  hand  in  a  splint  for 
a  considerable  time.  When  it  was  removed  the 
patient's  hand  presented  a  complete  picture  of  arthritis 
deformans ;  the  joints  were  not  merely  flexed  and 
stiffened,  but  completely  ankylosed.  All  the  other 
joints  of  the  body  were  perfectly  healthy,  and  the 
lady,  although  elderly,  was  quite  robust.  The  fact  that 
destructive  changes  took  place  in  the  joint  points  to 


182  ARTHRITIS 

an  injury  to  their  nerve-supply.  Simple  fixation  of 
the  joints  for  a  few  weeks  could  not  have  produced 
ankylosis  and  such  marked  deformity. 

In  all  cases  where  I  find  arthritis  deformans  as  a 
general  condition,  I  suspect  the  history  of  some  shock 
to  the  nervous  system  or  of  a  period  of  over-physical 
exertion  combined  with  mental  anxiety,  and  almost 
always  find  it.  Thus  a  woman  of  middle  age,  and  of 
apparently  healthy  constitution,  had  joints  which  were 
exceedingly  distorted.  She  was  the  wife  of  a  captain 
in  the  mercantile  marine,  and  was  accustomed  to 
voyage  with  her  husband.  On  one  occasion  during  a 
terrific  storm,  when  the  position  of  the  ship  appeared 
hopeless,  it  was  discovered  to  be  on  fire.  For  forty- 
eight  hours  she  did  not  know  whether  she  would  be 
drowned  or  burnt  to  death.  Immediately  afterwards 
the  joint  trouble  commenced  and  the  joints  became 
distorted.  There  was  no  history  of  rheumatism,  nor 
evidence  of  lithates. 

The  fact  that  nervous  shock  can  produce  a  serious 
disease  of  the  joints,  and  may  in  a  modified  form  greatly 
injure  their  nutrition,  should  be  taken  into  account  when 
delicate  women  are  ordered  to  have  all  their  teeth 
removed  in  the  hope  that  it  may  favourably  influence 
some  joint  trouble.  We  have  no  evidence  to  show 
that  bacilli  can  initiate  joint  disease  ;  but  we  have 
abundant  evidence  that  nervous  shock  can  do  so. 

I  do  not  know  of  any  treatment  which  will  cure  true 
arthritis  deformans.  In  ordinary  cases,  where  a  local 
or  general  asthenic  conditions  gives  rise  to  deformity, 
much  can  be  done  by  appropriate  splints  to  prevent  it. 
It  must  be  remembered  that  the  disease  is  not  pro- 
gressive, but  comes  to  a  natural  termination  after  a 
time.  A  large  number  of  the  cases  I  see  are  no  longer 


GONORRHCEAL   RHEUMATISM  183 

suffering  from  the  disease,  but  from  its  after-effects, 
which  are  purely  physical  and  may  be  improved  by 
physical  methods.  Many  of  these  patients  have 
received  vaccine  treatment  long  after  the  original 
disease  had  ceased. 

We  may  call  arthritis  deformans  incurable  because 
we  cannot  overcome  the  physical  ravages  it  leaves  ; 
but  it  is  really  a  disorder  which  comes  to  a  natural 
termination,  and  is  not  so  progressive  as  ordinary 
chronic  rheumatism. 

GONORRHCEAL  RHEUMATISM. 

There  is  one  form  of  joint  disease  in  which  the  influence 
of  bacilli  in  increasing  the  severity  of  the  symptoms, 
altering  the  character  of  the  inflammation,  and  pro- 
longing its  duration,  is  unquestionable.  This  is  gonor- 
rheal  rheumatism.  The  effect  of  the  gonococcus  is  to 
produce  considerable  effusion  round  the  joints,  and,  in 
cases  where  the  streptococcus  is  also  present,  the  tissues 
round  the  joints  become  very  puffy,  so  as  to  make  the 
swelling  appear  greater.  But  the  gonococcus  cannot 
be  regarded  as  the  cause  of  the  attack,  because  not  one 
patient  in  a  hundred  whose  tissues  are  invaded  by  it 
develops  joint  symptoms.  Neither  does  it  usually 
happen  if  the  patient  has  a  well-marked  lactic-acid 
diathesis.  But  given  this  diatheses,  and  an  attack  ol 
gonorrhoea,  and  then  a  chill  to  check  the  excretion  of 
lactic  acid,  we  get  gonorrhceal  rheumatism. 

It  is  for  this  reason  that  while  two  of  the  factors  are 
very  common,  viz.,  the  lactic-acid  diathesis,  and  the 
invasion  of  the  gonococcus,  gonorrhoeal  rheumatism  is 
fortunately  a  comparatively  rare  joint  disease,  because 
it  requires  the  intervention  of  a  chill  or  some  cause 
which  checks  excretion.  This  indicates  that  all  persons 


184  ARTHRITIS 

with  gonorrhoea  should  be  warned  of  the  absolute 
•  necessity  of  avoiding  a  chill.  Thus,  a  soldier  with 
gonorrhoea  should  not  be  exposed  to  damp  conditions 
if  it  can  be  avoided.  If  in  such  cases  the  excretion  of 
lactic  acid  is  interfered  with,  and  an  acute  or  subacute 
rheumatism  follows,  the  presence  of  the  gonococcus 
has  a  very  disastrous  effect  upon  the  inflammation  of 
the  joints. 

If  such  cases  are  treated  in  the  early  stages  by  methods 
which  liberate  the  lactic  acid  from  the  tissues,  they 
give  very  little  trouble  ;  but  if  the  action  of  the  gono- 
cocci,  and  the  presence  of  the  acid  in  the  tissues,  are 
allowed  to  continue,  destructive  changes  may  take 
place  in  the  joints  and  permanent  injury  result. 

In  one  case,  where  I  saw  the  patient  within  fourteen 
days  of  the  commencement  of  the  attack,  the  knees 
were  chiefly  affected,  and  the  bursa  above  the  knee- 
joint  on  both  knees  was  enormously  distended  with 
fluid.  In  this  case  I  gave  pyretic  treatment  to  remove 
the  lactic  acid,  and  at  the  same  time  adopted  a  treat- 
ment which  may  be  regarded  as  a  modified  vaccine 
method.  With  a  large  syringe  I  drew  off  the  fluid 
from  the  enlarged  bursa,  removing  all  that  I  could 
bring  away.  I  then,  without  removing  the  needle, 
after  sterilizing  the  syringe,  injected  a  1-2000  solution 
of  biniodide  of  mercury  (dissolved  with  iodide  of 
potassium)  into  the  sac.  My  theory  was  that  this  would 
destroy  the  gonococci  present  in  the  sac,  and  these 
would  act  as  an  autogenous  vaccine.  Whether  my 
theory  is  correct  or  not,  the  results  were  very  remark- 
able. At  the  end  of  three  weeks  the  patient's  knees 
were  practically  normal,  and  he  was  able  to  resume  his 
occupation  and  had  no  further  trouble.  The  effusion 
round  the  affected  joints  makes  the  treatment  quite 


ARTHRITIS   OF   THE  HIP- JOINT  185 

practical  in  all  cases,  and,  when  seen  before  destructive 
changes  have  occurred,  the  results  are  good. 

I  am  rather  afraid  of  gonococcal  vaccine,  for  I  had 
one  case  of  mild  gonorrhreal  rheumatism  in  a  young 
undergraduate  where  it  had  been  used  by  a  physician 
to  whom  he  was  taken,  and  the  result  was  disastrous. 
Not  only  was  there  no  improvement  in  the  joint  sym- 
ptoms, but  he  developed  rupia,  which  covered  the  whole 
body,  including  the  face.  The  boy  was  in  a  terrible 
condition.  If  vaccines  are  used  in  these  cases  it  appears 
advisable  that  these  should  be  autogenous,  as  it  is 
difficult  to  be  sure  of  the  purity  of  a  vaccine  taken  from 
another  individual.  I  think  the  method  that  I  have 
suggested  will  be  found  more  practical  as  well  as  safer ; 
but  I  do  not  think  it  would  be  of  the  same  value  unless 
steps  were  taken  at  the  same  time  to  remove  the  cause 
of  the  rheumatic  symptoms,  i.e.,  the  acid  in  the  tissues. 

ARTHRITIS    OF    THE    HIP-JOINT. 

The  chronic  diseases  which  affect  the  hip-joint  differ 
very  materially  from  those  we  find  in  the  other  joints. 
True  rheumatoid  arthritis  may  attack  the  hip-joint, 
and  when  it  does  so  it  is  usually  one  of  the  last  joints 
attacked  by  the  disease,  and  therefore  offers  no  difficulty 
as  regards  diagnosis.  The  hip- joint  may  also  be  the 
site  of  lithic  deposits,  but  less  commonly  than  the  joints 
which  are  more  exposed.  The  forms  of  chronic  hip 
disease  that  come  most  frequently  under  my  notice  are 
usually  not  associated  with  disorder  of  other  joints, 
and  may  occur  in  cases  where  no  other  joint  trouble 
exists.  The  term  'arthritis  of  the  hip'  is  used  to 
describe  both  these  diseases  ;  but  they  are  very  distinct 
in  their  pathology  and  symptoms. 

The  first  I  call  atrophic  disease  of  the  hip,  because  it 


186  ARTHRITIS 

is  due  to  atrophic  changes  in  the  head  of  the  femur, 
which  gradually  becomes  absorbed.  It  is  usually 
regarded  as  a  disease  of  advanced  age.  I  think,  how- 
ever, the  first  symptoms  commence  soon  after  middle 
life  ;  but  it  is  so  slow  in  development,  and  so  obscure 
in  its  physical  signs,  that  it  is  rarely  discovered  until 
late  in  life.  There  is  at  first  very  slight  pain  on  com- 
mencing to  walk  ;  this  disappears  very  soon,  and  the 
patient  is  able  to  take  a  long  walk.  After  a  time  any 
extra  exertion  is  followed  by  pains  in  the  thigh,  which 
may  come  on  during  the  night.  Some  time  elapses 
before  this  symptom  makes  it  necessary  to  curtail  the 
daily  walk. 

If  at  this  stage,  when  perhaps  the  disorder  has  existed 
for  two  years,  a  physical  examination  is  made,  the 
results  are  wholly  negative.  The  patient  has  perfect 
freedom  of  movement  of  the  joint,  and  there  is  no 
crepitation  or  pain  elicited  by  any  movement.  After 
a  time,  a  very  characteristic  symptom  develops.  The 
patient  on  rising  from  a  chair,  makes  an  almost  imper- 
ceptible pause  before  he  commences  to  walk.  As  the 
case  goes  on,  crepitation  can  generally  be  elicited 
by  flexing  the  extended  limb  on  the  body,  and  then 
offering  strong  resistance  as  the  patient  extends  it. 
During  this  time  the  pain,  chiefly  referred  to  the  thigh, 
increases  after  slight  exertion.  No  points  of  tenderness 
will  be  found  in  the  lumbar  plexus  or  the  nerves  of  the 
thigh.  There  is  gradual  shortening  of  the  affected 
leg,  with  some  eversion  of  the  foot ;  but  during  the 
whole  time  the  free  movement  of  the  hip  is  maintained  ; 
it  never  becomes  ankylosed  or  even  stiff. 

I  believe  that  the  disease  is  due  to  pressure  on  the 
obturator  nerve  in  the  pelvis,  causing  an  asthenic  con- 
dition of  the  branch  which  supplies  the  head  of  the 


ARTHRITIS  OF   THE  HIP- JOINT  187 

femur.  When  it  occurs  on  the  left  side  I  consider  it 
is  frequently  due  to  chronic  constipation.  There  are 
numbers  of  people  who,  in  spite  of  a  daily  evacua- 
tion, have  always  a  loaded  lower  bowel.  In  one  case, 
where  it  occurred  on  the  right  side  in  a  lady,  there 
was  the  history  of  an  abscess  in  the  pelvis  as  a  result 
of  appendicitis. 

In  these  cases  rest  of  the  hip- joint  is  essential.  I 
have  devised  some  mechanical  appliances ;  but  on  the 
whole  I  think  if  the  patient  can  be  induced  to  use 
crutches,  and  so  remove  the  weight  from  the  joint,  and 
use  a  Merlin  chair  for  indoor  use,  the  requirements 
are  sufficiently  met.  But  patients  will  rarely  submit 
to  the  treatment  until  the  disease  has  reached  an 
advanced  stage.  In  one  case,  where  I  recommended  it 
and  persuaded  the  patient  to  give  up  having  useless 
courses  of  treatment,  I  did  not  see  her  again  for 
some  years.  Then  a  physician,  with  whom  I  was 
lunching  in  London,  asked  me  to  see  a  patient  of 
his.  It  was  this  lady,  who  had  been  trying  one 
treatment  after  another  since  she  had  seen  me, 
and  was  steadily  getting  worse.  I  have  had  a  few 
cases  where  rest,  persevered  with  for  two  years,  has 
arrested  the  disease,  so  that  no  further  trouble  was 
experienced.  In  all  cases  rest  is  necessary  to  relieve 
pain. 

There  is  another  form  of  arthritis  which  I  call  hyper- 
trophic  disease  of  the  hip-joint.  This  is  the  more  common 
of  the  two.  It  usually,  but  not  invariably,  comes  on 
after  an  injury,  and  consists  of  a  general  hypertrophy 
of  the  bones  forming  the  hip-joint.  It  is  attended  by 
stiffness  in  the  joint  from  the  first,  and  the  range  of 
movement  is  gradually  diminished.  While  rest  may 
relieve  pain,  it  is  less  necessary,  because  ankylosis  of 


188  ARTHRITIS 

the  hip  is  the  natural  cure,  and,  when  this  happens, 
pain  ceases. 

One  patient,  a  lady,  had  this  disease  in  both  hips,  and 
the  pain  was  very  acute.  I  devised  a  splint  which,  by 
keeping  the  joints  at  rest,  gave  relief.  Now  both  hips 
are  ankylosed,  and  there  is  entire  absence  of  pain.  She 
can  walk  fairly  well,  and  can  even  manage  to  mount 
stairs  by  twisting  the  body  as  she  mounts  them. 

CHRONIC    SYNOVITIS    OF   THE    KNEE-JOINT. 

A  number  of  patients  come  under  my  observation 
with  pain  in  the  knee-joint  which  is  aggravated  by 
walking  and  descending  a  hill.  In  many  of  these  cases 
there  is  no  marked  swelling  of  the  joint ;  but  if  the 
knee  is  flexed  upon  itself  and  palpated,  there  will  be 
found  a  marked  tension  or  even  bulging  on  either  side  of 
the  ligamentum  patellae,  just  below  the  condyles  of  the 
femur.  This  indicates  the  presence  of  fluid  in  the  joint, 
which  has  escaped  observation  because  it  gives  no 
evidence  of  its  presence  when  the  joint  is  examined  in 
the  ordinary  manner.  These  cases  have  usually  been 
diagnosed  as  arthritis,  and  a  grave  prognosis  given. 
Many  of  them  have  been  treated  by  ionization  with- 
out result,  also  by  local  hot-air  baths  and  the  local 
application  of  iodine. 

The  most  efficient  treatment  is  the  application  of 
two  blisters  over  the  sites  of  the  swelling.  This  removes 
the  fluid  and  practically  cures  the  condition  in  forty- 
eight  hours ;  but  it  must  be  remembered  that  when 
the  fluid  has  been  a  source  of  irritation  over  a  long 
period  the  tissues  of  the  joint  remain  irritable,  and  a 
period  of  rest  should  follow  the  blister  until  this  has 
wholly  subsided.  In  some  cases  I  have  seen  serious 
mischief  to  the  structures  of  the  joint  from  the  result 


CHRONIC  SYNOVITIS  OF  THE  KNEE-JOINT    189 

of  a  little  fluid  left  after  an  attack  of  acute  synovitis 
from  any  cause.  While  inflammation  exists  the  fluid 
is  absorbed,  but  in  the  absence  of  inflammation  the 
synovial  membrane  appears  to  be  incapable  of  absorb- 
ing the  fluid,  and  it  may  remain  in  the  joint  to  be  a 
source  of  irritation  for  years,  unless  there  is  a  return  of 
the  acute  symptoms. 

Some  patients  with  persistent  pain  in  the  knee-joint, 
worse  on  walking,  and  who  have  no  fluid  in  the  joint, 
are  suffering  from  a  subacute  inflammatory  condition 
which  has  not  been  detected,  with  the  result  that  all 
treatments  have  failed,  because  the  patient  has  been 
walking  with  an  inflamed  joint  during  the  whole  of  the 
treatment,  so  that  a  mechanical  obstacle  to  cure 
existed.  This  can  always  be  avoided  if  the  surface 
temperature  of  the  joint  is  taken  with  the  palm  of 
the  hand,  and  compared  with  the  tissues  above  and 
below,  as  a  routine  method. 

My  own  routine  method  of  examining  a  knee-joint 
is  first  to  take  the  surface  temperature,  next  fully 
flex  and  extend  the  joint,  and  finish  the  movement 
in  the  position  of  extreme  flexion  while  I  examine 
the  tension.  The  examination  occupies  less  than  a 
minute,  but  it  gives  information  about  lithates,  arthritic 
changes,  inflammation,  or  presence  of  fluid,  and  en- 
ables a  diagnosis  to  be  made  with  a  certainty  that 
would  be  lacking  if  we  had  only  an  %-ray  photograph 
to  guide  us. 

These  subacute  inflammatory  conditions  of  the  knee- 
joint,  especially  when  they  have  existed  for  a  long 
period,  do  not  yield  very  readily  even  when  absolute 
rest  is  given  to  the  joint.  I  generally  use  some 
counter-irritant  to  the  skin,  such  as  dilute  linimentum 
crotonis,  combined  with  a  continuous  compress,  which 


190  ARTHRITIS 

is  applied  warm  and  re-moistened  night  and  morn- 
ing. The  stimulating  liniment  is  applied  as  often  as 
is  necessary  to  maintain  an  eruption  without  causing 
dermatitis. 

It  must  be  remembered  that  pain  in  the  knee-joint 
may  be  merely  a  reflex  symptom  of  hip  disease.  I 
remember  one  case  of  an  elderly  man  who  had  been 
treated  in  two  hospitals  for  knee  trouble  and  loss  of 
power  on  walking.  I  was  asked  to  see  if  anything 
could  be  done  for  him  ;  but  I  noticed  that,  as  the  man 
walked  across  the  room,  though  the  trouble  was  in  his 
left  knee,  he  supported  himself  by  a  stick  held  in  the 
right  hand.  I  at  once  diagnosed  hip  disease,  as  if  the 
knee  had  been  at  fault  he  would  have  held  his  stick 
on  the  same  side,  whereas  in  hip  cases  the  patient 
always  holds  it  on  the  side  opposite  to  the  affected 
joint.  This  diagnostic  point  may  be  useful  in  such 
cases.  In  this  case  the  man  had  never  had  the  smallest 
pain  in  the  hip,  in  which  he  had  advanced  atrophic 
disease,  but  very  severe  pain  in  the  knee-joint,  and 
attributed  his  loss  of  power  in  walking  solely  to  the 
knee. 

COMPLEX     FACTORS     IN    JOINT     DISEASE. 

I  have  classified  the  various  arthritic  disorders  in 
accordance  with  the  types  usually  met  with  in  everyday 
practice.  It  will  be  seen  that  each  of  these  types  is  due 
to  some  definite  physiological  impairment,  or  some 
excess  or  deficiency  in  the  normal  constituents  of  the 
body.  But  we  have  to  remember  that  the  individual 
patient  who  may  have  one  or  other  of  these  factors 
producing  joint  troubles,  may  have  others  peculiar  to 
his  conditions  of  life  or  his  constitutional  condition,  or 
may  have  these  factors  in  a  greater  or  lesser  degree,  so 


COMPLEX   FACTORS   IN  JOINT  DISEASE   191 

that  the  symptoms  presented  differ  from  those  more 
commonly  met  with. 

Thus,  joint  troubles  due  to  depression  of  the  central 
nervous  system,  which  I  have  described  under  the 
name  arthritis  deformans,  and  which  show  no  excess 
or  diminution  of  lactic  acid  or  phosphate  of  lime,  are 
comparatively  rare.  But  we  meet  with  this  neurosis 
in  patients  of  the  lactic  acid  and  lithic  diatheses.  They 
have  been  exposed  to  severe  shock  or  prolonged  over- 
strain of  the  nervous  system,  and  we  see  the  results  of 
this  in  the  condition  presented  by  the  joints.  In  these 
cases  the  deformity  is  a  factor  superadded  to  the  normal 
symptoms. 

A  patient  with  chronic  rheumatism,  chronic  gout,  or 
rheumatic  gout  may  have  a  sound  constitution  and  be 
of  a  robust  type  ;  but  persons  of  weak  constitution  and 
who  are  debilitated  may  suffer  from  these  disorders, 
and  consequently  the  joint  symptoms  may  have  greater 
resemblance  to  those  met  with  in  rheumatoid  arthritis, 
especially  if  there  has  been  great  wasting  of  muscle 
secondary  to  the  disuse  of  the  joints. 

Such  conditions,  while  they  may  make  an  accurate 
diagnosis  more  difficult  to  those  who  have  not  the 
opportunity  of  large  experience,  really  give  us  a  great 
amount  of  information  apart  from  anything  the  patient 
tells  us.  The  diagnosis  is  easier  and  more  accurate  if 
we  do  not  start  with  the  idea  that  we  have  to  give  a 
name  to  the  disease,  but  only  concern  ourselves  with 
what  is  actually  wrong  with  the  structures  of  the  joint, 
and  the  condition  of  the  excretory  functions  of  the 
skin.  We  have  to  decide  whether  a  deformity  is  due 
to  failure  of  the  muscular  apparatus  from  disease  or 
abnormal  use  of  its  function,  or  to  some  disorder  of  the 
central  nervous  system. 


192  ARTHRITIS 

When  we  have  made  our  minds  clear  on  these  points, 
we  are  in  the  best  condition  to  consider  the  treatment 
of  the  individual  case.  Thus,  although  we  may  be 
impressed  with  the  value  of  some  particular  dietary  in 
patients  who  have  lithates  in  their  joints,  we  shall  not 
at  once  put  every  patient  on  such  diet,  without  regard 
to  the  fact  that  they  may  be  too  thin,  or  too  fat,  or 
whether  they  eat  largely  or  too  little.  We  may  be 
impressed  with  the  value  of  exercise  in  the  same  class  of 
cases,  but  we  should  not  encourage  patients  whose  joints 
present  neurosal  symptoms  to  overfatigue  themselves. 

There  are  large  numbers  of  arthritic  patients  who  are 
best  treated  with  abundant  food  and  tonics,  but  there 
are  many  to  whom  the  same  treatment  would  do  great 
harm. 

We  cannot  differentiate  these  cases  by  the  name  we 
give  to  the  disorder,  but  by  the  physiological  conditions 
present  in  the  individual  patient. 

The  literature  of  this  subject  contains  too  much 
sweeping  generalization,  an  effort  to  find  a  common 
cause,  and  therefore  a  common  name,  for  symptoms 
which  result  from  conditions  often  the  reverse  of  one 
another,  and  which  require  recognition  before  efficient 
treatment  can  be  prescribed. 

The  result  of  this  is  not  only  failure  of  the  methods 
adopted,  but  the  practitioner  comes  to  regard  such 
cases  as  lacking  in  interest  and  undesirable  in  the  wards 
of  a  hospital.  As  a  matter  of  fact,  each  case  is  an 
interesting  problem  demanding  skill  and  judgement  on 
the  part  of  the  physician.  In  acute  disease  he  has 
always  the  vis  medicatrix  natures  to  help  him  in  accom- 
plishing his  cure ;  in  these  cases,  nature  has  failed,  and 
successful  results  represent  medical  skill  and  add  to  the 
reputation  of  the  profession. 


193 


CHAPTER    XI L 

1  NEURITIS.' 

DURING  recent  years  the  term  neuritis  has  been  used 
indiscriminately  to  represent  pain  in  any  part  of  the 
body,  and  therefore  the  word  conveys  no  information 
concerning  the  tissues  involved,  nor  does  it  give  any 
indication  for  treatment.  The  word  'neuritis';,  in  its 
literal  sense,  implies,  of  course,  that  the  patient  is 
suffering  from  inflammation  of  a  nerve.  This  is  a  very 
rare  affection,  and  does  not  come  under  my  observation. 

1  propose  to  consider  those  cases  which  have  been 
diagnosed  as  neuritis,  and  also  some  due  to  nerve 
disturbance  but  not  recognized  as  such.  They  can  be 
conveniently  divided  into  two  classes  :  (i)  Those  where 
the  site  of  the  pain  is  the  site  of  the  disorder  ;  (2}  Those 
in  which  the  site  of  the  disorder  does  not  correspond 
with  the  site  of  pain. 

In  the  first  class  we  may  place  rheumatism  affecting 
the  fibrous  tissue  of  muscles,  rheumatism  of  tendons, 
and  lithates  in  the  same,  and  rheumatism  in  the  sheath 
of  the  nerve-trunks.  In  all  of  these  tenderness  is  felt 
at  the  site  of  pain  when  the  part  is  pressed  upon.  This 
is  not  in  itself  a  diagnostic  symptom  ;  but  it  enables  us 
to  locate  by  manipulation  the  particular  tissue  affected. 
Thus  in  muscular  rheumatism  the  tenderness  is  diffuse 
and  usually  superficial.  In  rheumatism  of  tendons  it  is 
strictly  localized  to  the  tendon  or  tendons  involved. 
In  rheumatism  of  the  sheaths  of  nerves  it  can  only  be 
found  on  deep  pressure  over  the  nerve-trunk,  and  the 

13 


194  NEURITIS 

area  of  tenderness  is  limited  to  the  affected  tissue.  In 
all  these  cases  pain  can  be  elicited  by  any  movement 
which  puts  the  affected  tissue  on  the  stretch  ;  in  the 
case  of  muscular  rheumatism  by  any  effort  which 
brings  the  muscles  into  action.  It  is  the  power  to  pro- 
duce pain  by  stretching  the  tissue  which  distinguishes 
these  affections  from  some  others  which  I  shall  presently 
consider. 

Muscular  rheumatism  is  so  easily  diagnosed  that  it 
would  seem  impossible  for  any  mistake  to  be  made ; 
yet  the  large  majority  of  cases  1  have  seen  during  recent 
years  have  been  diagnosed  as  neuritis.  One  case 
which  I  saw  many  years  ago  impressed  me  very  much 
with  the  necessity  of  physical  examination  before  a 
diagnosis  is  given.  The  patient  was  a  London 
physician  who  had  suffered  very  intense  pain  in  the 
back  and  limbs,  for  which  he  had  failed  to  find  relief. 
He  had  tried  many  forms  of  treatment,  without  result, 
and  was  worn  out  with  pain  and  loss  of  sleep.  On  the 
morning  I  saw  him  he  had  written  letters  giving  up 
his  house  and  practice,  as  he  felt  that  he  would  never 
be  fit  for  work  again.  A  brief  examination  showed 
that  he  had  a  severe  attack  of  muscular  rheumatism; 
in  other  words,  the  fibrous  tissues  of  the  muscles  were 
loaded  with  lactic  acid  undergoing  oxidation.  I  gave 
the  opinion  that  he  would  be  able  to  resume  his  practice 
within  three  weeks.  He  resented  my  diagnosis  in 
spite  of  the  favourable  prognosis,  and  mentioned  the 
names  of  three  distinguished  physicians  who  had  dia- 
gnosed his  case  as  neuritis.  But  neither  of  them  had 
made  any  attempt  at  physical  examination.  I  ordered 
daily  pyretic  treatment,  and  a  fortnight  later  the 
patient  resumed  his  practice ;  he  wrote  me  some  years 
later  to  say  that  he  had  had  no  return  of  the  trouble. 


NEURITIS  195 

Rheumatism  of  the  tendons  and  fibrous  tissues  may 
be  the  result  of  a  chill,  but  more  frequently  some  strain 
upon  the  tissue  is  the  direct  cause.  This  is  most  likely 
to  happen  in  persons  who,  not  being  accustomed  to 
great  muscular  efforts,  try  to  accomplish  something 
greater  than  their  capacity,  or  are  forced  to  do  so  by 
some  accident.  The  primary  effect  of  the  strain  is  to 
depress  the  physiological  activity  of  the  tissue  ;  this 
causes  lactic  acid  to  accumulate,  but  during  this  period 
no  symptoms  are  experienced.  It  is  only  when  reaction 
occurs,  which  may  be  some  time  later,  that  pain 
develops. 

Certain  cases  of  sciatica  are  due  to  rheumatism 
affecting  the  sheath  of  the  nerve,  and  these  cases  are 
most  often  due  to  sitting  on  a  damp  surface.  A  vehicle 
in  which  the  cushioned  seat  has  been  exposed  to  rain, 
and  then  the  surface  has  dried,  so  that  the  dampness 
is  not  recognized,  is  one  of  the  most  frequent  causes  of 
this  painful  ailment.  It  is  readily  diagnosed  from  the 
fact  that  if  the  extended  limb  is  flexed  upon  the  body, 
so  as  to  stretch  the  nerve,  acute  pain  is  produced. 
Tenderness  over  the  nerve-trunk  is  also  found  if  deep 
pressure  is  made  at  a  point  mid-way  between  the  great 
trochanter  and  the  tuberosity  of  the  ischium.  None 
of  these  cases  present  any  difficulty  in  diagnosis. 

In  the  second  class  of  cases,  pain  may  be  complained 
of  in  a  limb,  or  at  some  part  of  the  body ;  the  cause 
of  the  pain  or  disability  may  not  be  readily  understood, 
and  the  term  neuritis  applied  to  it. 

If  we  take  cases  called  neuritis  of  the  arm,  where 
very  severe  pain  may  be  felt,  we  shall  usually  find  it 
due  to  one  of  two  conditions.  The  first  is  the  decom- 
position of  some  small  lithic  deposit  at  the  shoulder- 
joint  :  the  region  at  or  near  the  acromioclaviciilar 


196  NEURITIS 

articulation  is  a  frequent  site.  The  patient  is 
conscious  only  of  the  pain  radiating  down  the  arm, 
and  is  not  aware  of  a  point  of  acute  tenderness  in 
the  shoulder  which  may  frequently  be  covered  by 
the  finger-tip.  In  these  cases  a  branch,  probably,  of 
the  circumflex  nerve,  crosses  the  area  of  inflammation 
and  sets  up  irritation  in  the  main  nerve-trunk,  which 
makes  itself  evident,  not  in  the  nerve-trunk  itself, 
but  at  the  area  of  its  distribution.  Pain  is  frequently 
felt  at  the  point  of  the  insertion  of  the  deltoid 
muscle,  and  before  the  advent  of  the  word 
'neuritis'  this  pain  was  frequently  called  deltoid 
neuralgia. 

Now  it  is  obvious  in  these  cases  that  treatment 
administered  to  the  site  of  pain  can  accomplish  no 
good  results,  while,  if  we  treat  the  point  of  irritation 
at  the  joint  by  soothing  and  anodyne  applications, 
excellent  results  are  obtained.  After  the  acute  sym- 
ptoms have  passed,  I  find  it  a  good  plan  to  paint  the 
part  where  the  lithitis  exists  with  liniment  of  iodine, 
allow  it  to  dry,  and  then  cover  it  with  zinc  plaster.  In 
severe  cases,  where  there  is  some  effusion,  I  use  a  blister, 
which  gives  relief. 

In  these  cases,  although  the  pain  is  excited  by  a  sub- 
acute  inflammatory  process,  there  is  no  inflammation 
of  the  nerves  which  cause  the  pain,  so  that  the  word 
'  neuritis '  is  not  applicable :  '  lithitis '  or  '  gout '  is  a 
more  accurate  diagnosis. 

But  we  meet  with  cases  of  neuritis  in  the  arm  in 
which  the  lithate  plays  no  part.  There  is  pain  radiating 
down  the  arm  which  may  extend  to  the  fingers  ;  it  may 
be  more  or  less  severe,  and  have  a  paroxysmal  character. 
The  examination  of  such  a  case  is  never  complete  unless 
we  place  the  finger  immediately  above  the  upper  border 


NEURITIS  197 

of  the  clavicle  and  press  deeply,  and  then  carry  it  along 
the  bone  so  that  the  nerve-trunks  entering  into  the 
brachial  plexus  are  pressed  between  the  finger  and  the 
tissues  beneath.  One  or  more  points  of  great  tenderness 
may  be  revealed  by  this  proceeding,  although  the 
patient  is  wholly  unconscious  of  any  trouble  in  this 
region.  If,  without  relaxing  the  pressure,  we  move  the 
finger  to  and  fro  so  as  to  cause  friction  transversely 
to  the  nerve-trunk,  we  shall  excite  tingling  down  the 
arm  extending  to  the  finger,  and,  if  we  are  too  vigorous 
in  our  efforts,  acute  pain  will  be  produced,  or  an 
aggravation  of  the  pain  already  existing.  If  we  are 
more  gentle  in  our  friction,  and  continue  it  for  a  few 
minutes,  the  pain  caused  by  the  operation  gradually 
diminishes,  and,  if  the  patient  is  in  pain  at  the  moment, 
the  friction  gives  relief.  If  we  now  continue  the  process 
until  there  is  a  feeling  of  warmth  under  the  finger  owing 
to  increased  circulation,  which  may  take  from  seven  to 
ten  minutes,  the  pain  in  the  arm  is  relieved,  and  the 
part  to  which  the  friction  has  been  given  is  very  much 
less  tender  to  the  touch,  or  the  tenderness  may  altogether 
disappear,  whilst  the  increased  circulation  remains.  By 
this  simple  proceeding  we  are  able  to  demonstrate  the 
nature  of  one  of  the  most  important  causes  of  the 
symptoms  called  neuritis,  and  which  may  appear  in 
any  part  of  the  body. 

There  is  an  asthenic  condition  of  the  nerve-trunk, 
due  to  diminished  blood-supply.  This  condition  pro- 
duces no  symptoms  at  the  site  of  disorder,  but  causes 
pain  or  loss  of  nerve  power  at  the  point  of  distribution 
of  the  affected  nerve.  We  know  that  the  condition  is 
one  of  defective  blood-supply  to  the  nerve,  because,  as 
we  increase  the  circulation,  the  pain  in  the  area  of 
distribution,  and  the  tenderness  over  the  nerve-trunk, 


198  NEURITIS 

diminish,  or  are  temporarily  arrested.  It  is  obvious 
that  if  we  start  by  diagnosing  this  condition  as  neuritis, 
and  regard  these  symptoms  as  indicating  an  inflamma- 
tion of  the  nerve,  we  shall  resort  to  treatment  the 
opposite  to  that  which  is  beneficial,  and  finally  curative, 
and  we  shall  also  apply  our  remedies  to  the  area  of 
pain  instead  of  to  the  site  of  the  disorder.  In  other 
words,  the  diagnosis  '  neuritis '  centra-indicates  the 
necessary  and  curative  treatment. 

This  asthenia  of  the  nerve-trunks  is  one  of  the  most 
frequent  disorders  which  come  under  my  observation. 
I  do  not  think  there  is  a  single  nerve-trunk  in  the  spine 
which  I  have  not  seen  affected  in  this  manner.  The 
symptoms  produced  are  distant  from  the  site  of  trouble, 
and  if  the  cause  is  not  recognized  they  are  difficult  to 
account  for,  and  may  lead,  and  have  led,  to  errors  in 
diagnosis  of  a  serious  character.  The  diagnosis  of 
neuritis  is  not  the  worst  thing  that  can  happen  to  a 
patient  with  this  condition. 

The  cause  of  these  symptoms  is  unquestionably 
traumatic.  When  the  brachial  plexus  is  involved,  it 
is  a  consequence  of  some  act  of  exertion  in  which  the 
nerve-trunks  of  the  brachial  plexus  are  unduly  stretched. 
We  know,  when  a  ligament  is  sprained,  that  we  first 
of  all  have  acute  pain  and  some  effusion.  When  this 
has  subsided  and  the  use  of  the  joint  is  restored,  the 
site  of  the  injury  may  remain  in  an  asthenic  condition 
for  many  months,  although  the  patient  may  be  uncon- 
scious of  the  defect.  Under  these  conditions  lactic 
acid  may  collect  in  the  affected  tissues,  and  finally  there 
is  a  reaction,  and  rheumatic  symptoms  may  appear. 
Or,  in  the  patient  with  the  lithic  diathesis,  there  may 
be  failure  to  dissolve  the  dead  cells  of  the  tissues, 
and  lithates  may  form.  All  this  may  take  place  and 


NEURITIS  199 

present  no  symptoms  for  months  or  years  after  the 
accident. 

In  overstrain  of  a  tendon  from  some  act  of  exertion, 
the  symptoms  at  the  time  are  different.  There  is  not, 
of  necessity,  any  pain  at  the  time  of  strain,  or  the  sym- 
ptoms may  be  so  slight  as  not  to  excite  attention  or 
remain  in  the  memory.  But  the  physiological  con- 
sequences are  precisely  the  same  as  in  the  sprained 
ligament.  The  tendon  may  become  the  site  of 
rheumatic  trouble,  or  lithates  may  be  deposited. 

In  regard  to  sprain  of  the  sheath  of  a  nerve-trunk, 
there  may  be  pain  at  the  moment,  or  even  for  a  few 
days  later,  but  it  is  usually  transient.  This  pain  may 
be  felt  at  the  site  of  injury.  It  may  not  be  for  many 
months  after  the  injury  that  symptoms  begin  to  appear 
in  the  area  of  distribution  of  the  nerve,  less  frequently 
at  the  site  of  injury. 

The  asthenic  condition  which  occurs  in  ligaments  or 
tendons  has  a  natural  tendency  to  recovery,  because 
both  are  brought  into  functional  activity  during  the 
movements  of  the  body.  This  cause  of  natural  cure 
is  absent  in  the  trunks  of  nerves.  They  are  like  so 
many  insulated  wires  passing  through  the  tissues ;  the 
sheaths  of  the  nerves  take  no  part  in  their  functional 
activities,  and  receive  no  stimulus  from  them.  As 
a  result,  injuries  to  the  sheaths  of  nerve-trunks 
have  no  natural  tendency  to  recovery.  This  being 
so,  we  might  expect  the  symptoms  to  continue 
unabated  through  life,  but  this  is  not  the  case  ;  the 
patient  may  have  attacks  of  pain  or  disability  due 
to  loss  of  function  in  the  nerve,  and  this  may  last 
for  an  indefinite  period.  Then  there  may  be  periods 
during  which  the  patient  has  no  symptoms,  the  trouble 
is  apparently  cured,  but  from  time  to  time  they  recur, 


200  XEURITIS 

and  this  recurrence  is  always  in  the  same  area  as 
the  first  attack.  If,  however,  at  any  time  after  the 
injury,  whether  the  patient  has  symptoms  or  not,  we 
press  over  the  affected  nerve,  we  shall  find  a  point  of 
acute  tenderness,  showing  that  the  injury  remains 
although  no  symptoms  may  be  present. 

In  all  cases  of  pain  in  any  part  of  the  limb,  thorax, 
or  abdomen,  when  there  is  not  an  obvious  cause  for  it, 
the  back  should  be  examined. 

In  the  cervical  and  dorsal  regions,  a  line  may  be 
taken  about  two  inches  from  the  spines  of  the  vertebrae 
on  either  side.  The  finger  is  pressed  firmly,  and  a  to- 
and-fro  movement  made,  transversely  to  the  nerve,  as 
the  finger  is  carried  -down  the  spine.  This  will  only 
occupy  a  few  minutes.  The  brachial  plexus  is  best 
examined  immediately  above  the  clavicle  in  the  manner 
described,  or  friction  may  te  made  over  the  nerves  in 
the  axilla. 

The  lumbar  plexus,  which  is  more  subject  to  trau- 
matism  than  any  other  nerve-trunks,  will  show  an 
area  of  tenderness,  if  we  take  a  line  from  the  crest 
of  the  ilium  to  the  vertebral  column,  and  press  about 
two  inches  below  the  centre  of  this  line.  The  sacral 
plexus  is  easily  examined  by  deep  friction,  about  two 
and  half  inches  from  the  centre  of  the  bone  on  either  side. 

Injuries  of  the  lumbar  plexus  occur  with  greater 
frequency  than  those  of  other  nerve  trunks  because  it 
is  apt  to  be  sprained  by  twisting  the  body  in  an  effort 
to  save  a  fall.  In  many  cases,  where  the  patient  has 
a  fall,  and  may  be  severely  bruised,  the  local  injury  is 
of  far  less  consequence  than  the  injury  to  the  nerve- 
trunk,  which  may  give  no  evidence  of  its  existence 
for  months  or  years  later.  Both  lumbar  plexi  may  be 
sprained  by  the  attempt  to  lift  a  heavy  weight  with  the 


NEURITIS  201 

body  in  a  flexed  position.  Thus,  leaning  across  a  bed 
and  trying  to  lift  a  patient  may  cause  this  injury. 

The  symptoms  produced  by  these  injuries,  when  they 
appear,  will  be  pain  in  the  area  of  distribution  of  the 
nerve  affected,  and  it  is  a  diagnostic  symptom  in  these 
cases  that  the  nerve  which  conducts  the  pain  is  tender 
on  pressure.  Thus,  when  the  lumbar  plexus  on  one 
side  is  injured,  both  the  external  and  internal  cutaneous 
nerves  of  the  thigh  are  tender  to  pressure,  or  to  friction 
over  them.  The  best  point  to  examine  the  external 
cutaneous  nerve  is  at  a  point  mid-way  between  the 
great  trochanter  and  the  external  condyle  of  the  femur. 
The  internal  cutaneous  nerve  is  most  superficial  at  a 
point  about  four  inches  above  the  internal  condyle 
of  the  femur,  on  the  inner  side  of  the  thigh. 

Some  years  ago  the  statement  was  made  that  it  was 
impossible  to  distinguish  between  the  symptoms  of 
stone  in  the  kidney  and  lumbar  neuralgia.  If  by 
lumbar  neuralgia  we  mean  the  class  of  case  I  am 
describing,  the  diagnostic  symptom  is  that  in  this 
affection  the  internal  or  external  cutaneous  nerves, 
or  both,  will  be  tender  to  the  touch  ;  in  pain  caused 
by  stone  in  the  kidney  this  does  not  happen. 

It  is  less  common  to  have  pain  at  the  site  of  injury 
in  cases  of  traumatism  to  the  nerve-trunks.  There  can 
be  little  doubt  that  lactic  acid  accumulates  in  the 
fibrous  tissues  of  the  sheath  of  the  nerve,  and  by  its 
presence  may  cause  thickening,  and  thus  interfere  with 
the  nutrition  of  the  nerve.  I  called  attention  to  the 
fact  that  the  thickened  cell-wall  in  chronic  rheumatism 
was  one  of  the  causes  of  the  wasting  of  muscles  and  the 
tissues,  and  some  interference  with  the  nutrition  of 
the  nerve  must  occur  if  the  walls  of  its  sheath  are 
thickened  from  the  same  cause.  Except  in  the  case  of 

cour  v- 


202  NEURITIS 

the  sciatic  nerve,  which  is  stretched  in  certain  move- 
ments of  the  body,  there  is  nothing  to  excite  reaction 
in  the  nerve-trunk.  The  thickening  of  the  sheath  with 
its  local  tenderness  may  remain  for  twenty  or  thirty 
years  without  any  local  pain  being  exhibited  in  the 
nerve-trunk,  although  pain  in  its  area  of  distribution 
may  be  frequent  or  recurrent. 

I  have  met  with  some  exceptions.  One  was  that  of 
a  lady  resident  in  a  distant  colony  who  was  seized  with 
most  acute  pain  in  the  lumbar  region  on  both  sides  and 
involving  the  hips.  The  pain  was  so  acute  that  the 
patient  had  to  be  kept  under  the  influence  of  morphia. 
When  she  had  sufficiently  recovered  she  was  sent 
to  London  for  examination,  as  the  symptoms  were 
obscure.  She  saw  one  of  our  greatest  and  most 
experienced  surgeons,  who,  having  given  an  hour  to 
examining  her,  felt  uncertain  about  the  cause  of  the 
pain  and  disability,  and  asked  a  very  distinguished 
authority  on  diseases  of  the  nervous  system  to  see  her 
with  him.  They  finally  pronounced  it  a  case  of  acute 
arthritis  of  both  hips.  I  subsequently  saw  the  patient 
and  found  that  she  had  sprained  the  lumbar  plexus 
on  both  sides,  and  that  this  had  caused  severe  pain 
both  at  the  site  of  injury,  as  well  as  in  the  area 
of  distribution.  I  suggested  that  she  had  tried  to  lift 
a  weight  with  the  body  flexed  at  some  time  before  the 
symptoms  appeared.  She  strongly  insisted  that  this 
could  not  be  the  case,  as  she  was  too  old  for  any 
laborious  employment.  The  next  day  her  daughter 
called  to  tell  me  that  her  mother  had  since  recollected 
that  during  her  husband's  illness  she  had  tried  to  lift 
him  in  bed,  and  felt  a  severe  pain  in  her  back  ;  that  the 
pain  disappeared  in  a  few  days,  and  she  had  forgotten 
it.  It  was  four  or  five  months  after  this  that  the  severe 
attack  occurred. 

ffj~  I 


NEURITIS  208 

I  give  these  particulars  because  in  many  cases  the 
patient  will  deny  the  history  of  an  accident,  as, 
owing  to  the  lapse  of  time  between  the  symptoms 
and  the  cause,  no  impression  has  been  left  on  the 
mind. 

While  in  the  majority  of  cases  of  injury  to  the  lumbar 
plexus  there  is  pain  as  the  chief  symptom,  there  are 
some  in  which  it  is  absent  and  the  motor  fibres  of  the 
nerve  appear  to  be  alone  affected.  A  common  symptom 
is  that  the  knee  gives  way  whilst  walking,  and  the 
patient  falls  down  in  consequence.  This  is  due  to  a  lack 
of  nerve  power  in  the  internal  and  external  cutaneous 
nerves,  which  supply  the  structures  responsible  for 
supporting  the  joint.  The  symptoms,  both  of  pain  and 
loss  of  power,  depend  upon  diminution  of  the  normal 
functional  activity  of  the  nerve,  so  that  if  anything 
occurs  to  depress  the  general  nervous  system  it  will 
make  itself  evident  in  the  weakest  nerve.  Thus  a 
patient  with  injury  to  the  lumbar  plexus  will  walk 
quite  well  and  continue  to  do  so,  but  one  day,  from 
over-fatigue  or  some  cause  of  nerve  depression,  the 
knee  will  suddenly  give  way  and  the  patient  will 
fall  down.  This  symptom  does  not  usually  occur  in 
patients  who  suffer  pain  from  lumbar-plexus  injury, 
and  those  who  have  the  symptom  very  seldom  com- 
plain of  pain,  which  shows  that  the  sensory  fibres  are 
depressed  in  one  case  and  the  motor  in  the  other. 

As  I  have  stated,  the  symptoms  do  not  usually  appear 
until  a  considerable  time  after  the  accident  ;  but  I  had 
one  case  in  which  it  appeared  in  the  first  twenty-four 
hours.  An  elderly  lady,  whilst  walking,  came  to  a 
small  step  which  she  did  not  notice,  and  in  consequence 
fell  to  the  ground.  She  walked  home  and  felt  none 
the  worse  for  the  accident  ;  but  the  next  morning,  on 


204  NEURITIS 

rising  from  bed,  her  knee  gave  way  and  she  fell  to  the 
ground.  The  symptom  persisted,  and  two  surgeons 
had  been  consulted  before  I  saw  her,  and  could  find  no 
sign  of  injury.  But  when  I  touched  the  point  I  have 
mentioned,  the  pain  was  very  acute,  and  friction  over 
the  point  eventually  cured  the  trouble. 

Injuries  to  the  lumbar  plexus  may  cause  spasm  of 
the  muscles  of  the  hip  so  as  to  produce  a  shortening 
of  the  limb  on  the  affected  side.  One  case  of  this  kind 
came  under  my  notice  many  years  ago.  The  patient 
was  a  lady  27  years  of  age.  She  complained  of  severe 
neuralgia,  and  came  to  me  for  treatment  of  this  trouble. 
On  examination  I  found  that  she  had  a  pronounced 
lateral  curvature  of  the  spine,  and  one  leg  was  four  and 
a  half  inches  shorter  than  the  other.  She  was  wearing 
steel  supports  for  the  spine,  a  steel-support  from  the 
ankle  to  the  knee,  and  a  high  boot. 

I  formed  the  conclusion  that  the  original  condition 
had  been  produced  by  spasm  of  muscle  due  to  injury 
of  the  lumbar  plexus,  and  that  efforts  to  remedy  this 
by  mechanical  means  had  pushed  up  the  hip  and 
caused  the  condition  of  the  spine.  I  kept  the  patient  in 
bed  for  a  fortnight,  and  ordered  cold  sponging  to  the 
whole  spine  (which  was  irritable  to  percussion),  followed 
by  deep  effleurage  until  an  active  circulation  was  pro- 
duced ;  also  friction  over  the  lumbar  plexus  on  the 
affected  side.  I  then  put  traction  on  the  shortened 
limb  by  means  of  a  weight  and  pulley.  At  the  end  of 
the  sixth  week  the  scoliosis  and  the  shortening  of  the 
limb  had  disappeared ;  the  patient  was  able  to  walk 
without  any  supports,  and  quickly  resumed  active  life. 
She  had  been  for  some  years  under  the  treatment 
of  an  orthopaedic  surgeon,  who  did  not  recognize 
that  by  progressively  increasing  the  height  of  the  boot 


NEURITIS  205 

he  was  simply  tilting  the  pelvis  and  distorting  the 
spine.  There  was  no  real  shortening  of  the  leg  from 
the  first. 

Recently  I  had  two  cases,  at  the  same  time,  under 
treatment  where  injury  of  the  lumbar  plexus  had  pro- 
duced spasm  of  the  muscles  of  the  hip,  and  shortening 
of  the  limb  as  a  consequence.  One  was  an  ex-cavalry 
soldier,  who  had  so  much  swelling  and  pain  in  the  region 
of  the  hip,  combined  with  a  shortening  of  over  three 
inches,  that  at  the  hospital  from  which  he  was  sent  to 
me,  the  diagnosis  of  arthritis  of  the  hip-joint  was 
made.  Curiously  enough,  it  was  apparently  confirmed 
by  an  #-ray  photograph.  The  man  had  all  the  sym- 
ptoms of  an  advanced  case  of  arthritis  of  the  hip,  but 
the  disorder  had  only  existed  for  a  few  months.  He 
had  been  examined  for  tuberculosis  with  negative 
results. 

In  this  case  there  was  not  only  acute  tenderness  over 
the  lumbar  plexus,  but  pressure  produced  spasm  of  the 
muscles.  There  was  acute  tenderness  over  the  external 
and  internal  cutaneous  nerves  of  the  thigh.  Now  in 
cases  of  hip- joint  disease  we  may  have  pain  reflected 
by  these  nerves,  and  felt  both  in  the  thigh  and  the 
knee-joint,  but  the  nerves  themselves  are  not  tender 
to  the  touch.  I  at  first  thought  that  this  injury  was 
due  to  one  of  the  many  falls  he  had  had  from  his  horse, 
and  reported  this  opinion ;  but  subsequent  examination 
showed  that  both  lumbar  plexi  had  been  sprained,  and 
this  must  have  happened  from  lifting  a  heavy  weight. 
On  inquiry,  I  found  that  after  leaving  the  army  he  had 
been  in  attendance  upon  a  very  heavy  man  who  was  an 
invalid,  and  when  leaning  over  the  bed  and  trying  to  lift 
him  the  injury  had  taken  place.  In  this  case  vibration 
over  the  affected  nerve,  and  traction  by  weight  and 


206  NEURITIS 

pulley  at  a  later  stage  of  treatment,  quite  removed  all 
the  symptoms,  and  the  man  was  restored  to  work. 

The  other  case  was  that  of  an  elderly  man  who  had 
sprained  the  left  lumbar  plexus  during  a  fall.  The  con- 
dition was  much  less  severe,  and  the  limb  of  the  affected 
side  which  was  shortened  by  two  inches  became  normal 
by  simple  rest  in  bed  and  treatment  of  the  affected 
nerves. 

Injuries  to  the  sacral  plexus  are  caused  by  a  fall  in 
the  sitting  posture.  They  are  far  less  frequent  than 
injuries  of  the  lumbar  plexus,  not  because  such  falls 
are  uncommon,  but  because  it  requires  a  severe  fall  to 
produce  the  injury.  One  severe  case,  involving  the 
nerves  on  both  sides,  was  due  to  a  lady  intending  to 
sit  on  the  box  seat  of  a  coach,  missing  the  seat,  and 
falling  to  the  ground  in  the  sitting  posture. 

The  pain  in  these  cases  follows  the  course  of  the 
sciatic  nerve,  and  this  nerve  is  tender  to  the  touch. 
This  is  also  the  case  in  rheumatism  of  the  sheath 
of  the  sciatic  nerve,  but  in  the  latter  case  pain  can 
be  produced  by  stretching  the  nerve,  as  when  the 
extended  leg  is  flexed  upon  the  body.  This  symptom 
does  not  occur  when  the  pain  is  due  to  injury  of  the 
sacral  plexus.  In  a  local  rheumatism  of  the  sheath 
of  the  nerve  the  pain  is  aggravated  by  walking ;  but 
this  symptom  is  not  so  prominent  in  injury  of  the 
sacral  plexus.  The  pain  is  apt  to  occur  when  at  rest, 
and  also  in  bed  ;  and  especially  after  fatigue.  There 
is  tenderness  on  pressure  over  the  sacrum  at  the 
points  where  the  nerves  emerge  which  is  not  present 
in  rheumatism  of  the  sheath  of  the  nerve ;  nor  is  it  in 
cases  of  pure  neuralgic  sciatica. 

These  cases  have  no  tendency  to  natural  recovery, 
and  the  baths  which  would  benefit  rheumatism  of  the 


NEURITIS  207 

sheath  of  the  nerve  may  quite  fail  to  relieve  the 
condition.  But  when  the  true  nature  of  the  disorder 
is  diagnosed,  the  fact  that  the  nerves  are  placed  more 
superficially  than  those  of  the  lumbar  plexus  makes 
them  more  easy  to  treat  by  physical  methods,  and 
rapid  improvement  takes  place. 

These  cases  are  very  interesting,  because  the  sym- 
ptoms indicate  the  nerve-trunk  affected,  and  the  possible 
causes  of  injury  to  special  nerve-trunks  are  limited,  so 
it  is  not  difficult  to  describe  an  accident  which  the 
patient  has  met  with  and  wholly  forgotten.  In  one 
case  there  were  tender  points  over  the  cervical  and 
dorsal  nerves,  and  also  over  the  left  lumbar  plexus. 
This  could  only  have  been  caused  by  the  patient  falling 
downstairs  on  her  back  and  then  something  occurring 
to  twist  the  body  to  one  side.  This  diagnosis  was 
confirmed  by  the  patient.  She  was  on  board  ship, 
twenty  years  before,  and  had  gone  on  to  the  upper 
deck  ;  as  she  was  descending  the  companion  ladder 
her  foot  slipped  and  she  came  down  the  steps  on  her 
back,  and,  just  before  she  reached  the  bottom,  someone 
trod  on  her  dress  and  she  twisted  over  and  reached 
the  deck  on  her  side. 

I  have  seen  many  cases  where  the  patient  was  liable 
to  attacks  of  acute  pain  of  rather  an  alarming  character 
in  the  region  of  the  heart.  In  such  cases  I  frequently 
find  a  tender  point  over  the  3rd  or  4th  dorsal  nerve, 
and  by  passing  the  finger  along  the  lower  border  of  the 
ribs  the  tender  nerve  can  be  traced  to  the  site  of  pain. 
Friction  over  the  affected  nerve  will  give  relief  during 
an  acute  attack,  and  if  the  nerve  is  treated  the  return 
of  this  trouble  may  be  avoided. 

In  all  obscure  pains  over  the  stomach  or  liver  which 
come  on  periodically  and  which  are  not  easily  accounted 


208  NEURITIS 

for  by  any  gastric  or  hepatic  cause,  the  region  of  the 
6th  and  7th  dorsal  nerves  should  always  be  examined, 
as  it  may  solve  the  whole  difficulty.  I  had  one  case 
in  which  the  8th  and  gth  dorsal  nerves  on  the  right  side 
were  affected,  causing  very  acute  and  continuous  pain. 
The  nerves  had  been  strained  whilst  playing  polo.  The 
patient,  a  naval  officer,  was  quite  relieved  by  treatment. 
Five  years  later  he  had  a  return  of  the  pain,  and  as  a 
consequence  abscess  of  the  liver  was  suspected  and  he 
narrowly  escaped  operation. 

Some  cases,  regarded  as  recurrent  appendicitis,  are 
due  to  injury  of  the  nth  and  I2th  dorsal  nerves  on  the 
right  side.  Acute  tenderness  over  these  nerves  will  be 
found.  If  this  condition  is  discovered  during  an  acute 
attack,  and  friction  is  given  to  them,  pain  will  be 
relieved  in  about  ten  minutes.  To  prevent  return  of  the 
trouble,  friction  should  be  given  daily  until  the  nerves 
are  no  longer  tender  to  the  touch. 

A  further  diagnostic  method  in  all  painful  affections 
of  the  abdomen  due  to  nerve  injury  is  to  pinch  up  the 
abdominal  wall  over  the  site  of  pain,  and  hold  it  firmly 
between  the  thumb  and  fingers  of  one  hand,  while 
pressure  and  a  rolling  movement  is  made  to  the  tissues 
with  the  other  hand.  This  means  that  the  abdominal 
contents  beneath  the  abdominal  wall  are  in  no  way 
affected  by  the  manipulation.  If,  then,  pain  is  pro- 
duced, we  know  that  it  is  due  to  the  nerves  of  the 
abdominal  wall,  and  not  to  any  inflammatory  condition 
of  the  intestine.  In  the  cases  I  have  described,  the 
abdominal  wall  will  always  be  found  tender  over  the 
site  of  pain. 

I  have  already  mentioned  that  patients  with  the 
lithic  diathesis  are  more  liable  than  others  to  recurrent 
pain  in  the  gall-duct,  due  to  thickened  bile  or  concretions, 


NEURITIS  209 

and  this  pain  is  frequently  reflected  to  the  region  of  the 
appendix.  Therefore,  in  cases  of  suspected  appendicitis, 
the  region  of  the  gall-bladder  should  always  be  exam- 
ined in  addition  to  lower  dorsal  nerves. 

In  one  lady  who  had  undergone  very  strenuous  and 
unaccustomed  exertions  during  the  war,  I  found  acute 
tenderness  over  the  8th  and  I2th  dorsal  nerves,  and 
also  over  the  lumbar  plexus,  all  on  the  right  side.  On 
account  of  pain,  the  right  ovary  and  the  appendix  had 
been  removed  ;  but  she  was  told  that  they  were  free 
from  disease.  A  further  operation  was  proposed  for 
'floating  kidney'.  The  abdominal  muscles  were  quite 
firm,  and  there  was  nothing  to  indicate  any  displace- 
ment of  the  kidney.  Pain  in  the  thighs  and  loss  of 
power  in  the  knee-joint  were  attributed  to  this  displace- 
ment of  the  kidney,  but  such  displacement  would  not 
cause  the  tenderness  and  asthenic  condition  of  the 
internal  and  external  nerves  of  the  thigh  which  existed 
in  her  case.  This  is  another  diagnostic  symptom, 
because  reflex  pains  are  not  accompanied  by  tender- 
ness over  the  trunks  of  the  conducting  nerves. 

These  facts  led  me  to  examine  the  corresponding 
nerves  on  the  left  side  of  patients  who  had  chronic 
colitis,  or  who  were  subject  to  repeated  attacks.  In  a 
large  number  of  cases  I  have  found  tenderness  over  the 
nth  and  i2th  dorsal  nerves  of  the  left  side  in  these 
cases,  and  also  I  have  found  treatment  of  these  nerves, 
when  tender,  produce  better  results  than  any  other 
method.  Previously  I  had  formed  the  conclusion  that 
colitis  always  represented  an  asthenic  condition  of  the 
nervous  system  and  that  no  local  treatment  was  of 
value  unless  the  general  health  was  restored.  I  think 
this  view  is  correct,  but  it  is  obvious  that  if  we  can  find 
a  definite  cause  for  the  local  asthenia,  and  remove  it, 

14 


210  NEURITIS 

the  results  of  treatment  will  be  much  more  rapid  and 
complete. 

The  cause  of  injury  to  these  nerves  in  the  ca- 
have  met  has  been  usually  the  effort  to  lift  some  heavy 
piece  of  furniture.  Thus,  a  young  lady  tried  to  move 
a  piano,  and  was  at  last  obliged  to  desist  because  the 
strain  was  too  great.  Her  sister  then  made  an  effort 
to  do  the  same  thing,  but  was  also  obliged  to  give  up. 
Both  these  ladies  developed  colitis  about  the  same 
time,  a  few  months  later. 

I  recently  had  a  man  under  treatment  who  was 
subject  to  severe  pain  in  the  region  of  the  descending 
colon,  and  also  to  great  distention  of  this  part 
of  the  intestine.  He  had  treatment  for  many  years, 
and  adopted  various  dietetic  measures  without  relief. 
I  found  marked  tenderness  over  the  nth  and  I2th 
dorsal  nerves  of  the  left  side.  I  found  that  he  was  the 
manager  of  a  large  piano  business,  and  he  admitted  that 
he  had  sometimes  helped  to  move  a  piano,  but  had  not 
attempted  it  since  he  had  this  trouble.  Treatment  of 
these  nerves  made  a  rapid  and  permanent  cure  of  his 
condition. 

Efforts  to  lift  a  weight  when  the  spine  is  flexed  are 
likely  to  strain  the  lumbar  plexus  ;  but  the  same  efforts, 
when  the  body  is  erect  and  close  to  the  object  to  be 
lifted,  appear  to  put  the  greatest  strain  on  the  lower 
dorsal  nerves. 

I  have  seen  other  cases  where  injury  to  nerve-trunks, 
and  especially  the  lumbar  plexus,  has  been  followed 
by  loss  of  motor  power,  particularly  during  fatigue  or 
in  depressed  conditions  of  the  nervous  system,  which 
has  led  to  the  diagnosis  of  sclerosis,  and  unnecessary 
alarm  caused  to  the  patients  and  their  friends. 

These  facts  point  to  the  necessity  of  examining  the 


NEURITIS  211 

condition  of  the  spinal  nerves  in  all  cases  where  pain 
and  disability  exist.  The  electrical  methods  adopted  by 
neurologists  are  not  adapted  to  the  discovery  of  these 
lesions.  Simple  pressure  and  friction  with  the  finger 
is  all  that  is  necessary  in  order  to  detect  them. 

The  same  is  true  in  regard  to  the  treatment  of  these 
disorders.  We  might  expect  that  having  to  deal  with 
an  affection  of  the  nerve,  we  should  find  electricity  our 
best  resource.  The  high-frequency  current  will  often 
relieve  pain,  and  the  galvanic  current  improve  the 
nutrition  of  the  nerve,  but  neither  of  these  will  take 
the  place  of  mechanical  friction  with  the  finger.  It 
requires  to  be  commenced  very  gently,  the  movement 
being  always  transverse  to  the  nerve,  and  the  pressure 
gradually  increased  as  the  functional  activity  of  the 
nerve  becomes  greater  and  the  tenderness  consequently 
less.  It  needs  to  be  continued  until  a  feeling  of  warmtii 
is  produced  in  the  part,  and  with  it  a  subsidence  of 
the  pain  and  tenderness.  This  treatment  usually  has 
to  be  continued  daily  for  three  weeks  or  a  month  in 
order  to  secure  curative  results. 

There  are  some  cases  in  which  the  tenderness  is  so 
acute  that  the  treatment  would  be  exceedingly  painful, 
and  as  a  routine  measure  it  is  desirable  to  commence 
the  treatment  by  electric  vibration  over  the  affected 
nerve.  If  the  vibrator  has  a  rotary  action  of  the 
applicator  which  is  checked  when  applied  to  the  body, 
the  energy  is  conveyed  to  the  tissues  and  a  rise  of 
temperature  takes  place.  This  does  not  happen  when 
the  rotation  of  an  excentric  wheel  simply  causes  a 
percussive  motion  to  the  applicator.  After  vibration 
has  raised  the  temperature  of  the  part,  friction  to  the 
nerve  becomes  painless,  and  can  be  done  much  more 
vigorously  than  when  it  is  not  used. 


212  NEURITIS 

While  there  are  some  cases  where  the  treatment  will 
succeed  without  other  measures,  there  are  others  where 
the  nerve-trunk  is  so  saturated  with  lactic  acid  that 
some  form  of  pyretic  treatment  should  be  given  at  the 
same  time.  In  fact,  the  best  results  are  always  attained 
in  this  way. 

The  immediate  effect  of  treatment  is  always  relief 
of  pain,  and  this  proves  that  it  is  indicated ;  but  no  case 
can  be  regarded  as  cured  until  the  nerve  is  no  longer 
tender  to  the  touch.  Thus  relief  of  all  the  symptoms 
is  not  of  necessity  a  cure.  While  the  nerve-trunk 
remains  tender,  there  is  always  liability  to  recurrence. 

The  term  '  neuritis '  cannot  be  properly  applied  to 
any  of  the  cases  I  have  described.  Pain  due  to  an 
asthenic  state  of  a  nerve,  this  condition  being  due 
to  a  mechanical  cause,  the  result  of  injury,  might 
be  called  traumalgia.  This  would  distinguish  it  from 
a  neuralgia,  which  might  be  cured  by  medicinal 
treatment.  Traumalgia  necessitates  local  treatment 
to  the  site  of  injury.  The  same  is  true  of  those 
cases  when  the  motor  fibres  of  the  nerve  are  alone 
affected,  and  the  symptoms  are  those  of  loss  of  power 
at  the  point  of  distribution.  Such  cases  might  be 
described  as  traumasthenia  of  the  particular  nerve 
affected.  In  both  cases  we  have  to  remember  that 
the  cause  of  the  continued  asthenia  of  the  nerve  is 
the  thickening  of  its  sheath,  and  that  we  have  to 
adopt  some  means  by  which  the  additive  lactic 
acid,  which  causes  the  pressure,  is  removed. 


213 


CHAPTER   XIII. 

THE    NURSE'S   PART   IN    TREATMENT. 

IN  the  chapter  on  Pyretic  Treatment  I  have  described 
some  of  the  simple  methods  by  which  the  conditions 
causing  the  '  rheumatic  '  attack  can  be  averted,  and 
which  may  also  be  used  with  advantage  when  acute 
symptoms  have  occurred.  But  when  the  changes  in 
the  tissues  have  reached  an  advanced  stage  and  the 
joints  have  become  crippled,  systematic  treatment  is 
necessary,  and  this  needs  efficient  appliances  and  also 
the  aid  of  nurses  specially  trained  for  this  work.  At 
the  Lansdown  Hospital  and  Nursing  Home  at  Bath  I 
have  had  a  long  experience  in  the  instruction  of  nurses 
in  carrying  out  treatment,  and  some  hints  on  the 
points  special  to  these  methods  may  be  useful  to  the 
practitioner. 

In  the  first  place  it  is  essential  that  the  nurse  should 
clearly  understand  the  physiological  effect  aimed  at  in 
any  treatment  she  has  to  administer.  For  this  reason 
it  is  desirable  that  they  should  be  selected  from  the 
educated  classes. 

They  must  learn  that  the  thermometer  is  not  an 
instrument  solely  used  for  detecting  the  presence  of 
fever  ;  but  that  it  is  the  most  valuable  means  we  possess 
of  estimating  the  activity  of  the  chemical  processes 
taking  place  in  the  body. 

Unless  it  is  made  an  absolute  rule  that  the  register 
of  the  thermometer  be  shaken  down  to  95°  F.  before 
the  temperature  is  taken,  the  subnormal  temperature 


214     THE    NURSE'S    PART    IN    TREATMENT 

will  not  be  recorded.  A  person  whose  temperature  is 
always  subnormal,  even  if- he  be  otherwise  in  good 
health,  has  that  condition  of  imperfect  metabolism 
which  may  lead  to  arthritic  developments.  If  the 
morning  temperature  suddenly  falls  during  treatment, 
it  most  usually  indicates  over-fatigue  on  the  previous 
day.  If  it  persists  in  spite  of  rest,  it  may  indicate  that 
the  treatment  itself  is  the  cause  of  fatigue  and  must 
be  modified.  In  such  cases  the  galvanic  bath  on 
alternate  days  with  the  thermal  couch  (or  pyretic  bath) 
is  usually  sufficient  to  correct  the  difficulty. 

It  will  be  noticed  that  few  patients  with  the 
rheumatic  or  lithic  diatheses  have  a  morning  temper- 
ature of  98' 4°  F.  unless  a  febrile  condition  is  present. 
By  the  words  '  normal  temperature '  we  mean  the 
temperature  normal  to  the  patient,  and  not  the 
theoretic  normal. 

Another  point  of  importance  is  the  difference  between 
the  morning  and  evening  temperature.  A  wide  varia- 
tion in  the  absence  of  any  febrile  condition  usually 
indicates  some  debility  ;  if  it  is  both  wide  and  erratic, 
it  points  to  fatigue  of  the  nervous  system. 

It  is  usual  with  patients  to  show  a  greater  variation 
at  the  commencement  of  treatment  than  as  it  continues, 
and  when  it  becomes  very  slight  indeed  we  can  be 
satisfied  that  the  patient's  nervous  equilibrium  has 
been  restored.  It  will  be  seen,  therefore,  that  the 
temperature  chart  of  a  patient  whose  temperature 
never  exceeds  the  '  normal '  line  is  very  instructive, 
and  helps  us  in  regulating  not  only  treatment  but  the 
daily  life  of  the  patient  both  as  regards  exercise  and 
nervous  excitement. 

Thus  one  patient  whose  temperature  was  subnormal 
suddenly  had  a  febrile  rise  every  night,  and  I  failed  to 


THE    NURSE'S    PART    IN    TREATMENT     215 

account  for  it.  On  close  examination  I  found  that 
she  played  bridge  every  afternoon  ;  I  stopped  this,  and 
the  temperature  became  normal. 

When  the  temperature  is  above  normal  it  is  important 
to  consider  it  in  relation  to  the  rate  of  the  pulse.  As 
a  rule  we  may  regard  a  rise  of  temperature  without 
any  great  acceleration  of  the  pulse  as  a  simple  hyper- 
thermia,  showing  active  chemical  change  of  a  beneficial 
character. 

A  rapid  pulse  with  a  moderate  temperature  is  very 
uncommon  in  such  cases,  but  when  it  occurs  we  may 
suspect  a  large  amount  of  free  lactic  acid  is  irritating 
the  vascular  system.  In  such  cases  the  skin,  if 
functionally  active,  shows  a  very  acid  reaction.  The 
free  use  of  some  simple  alkali,  such  as  bicarbonate 
of  soda,  may  then  prove  very  useful  and  control 
the  symptoms  ;  when  it  does  so,  we  know  that  our 
diagnosis  is  correct. 

In  all  cases  of  continued  fever,  during  acute  attacks, 
it  is  very  important  to  observe  the  skin  reaction  in 
relation  to  the  temperature.  If  the  latter  falls  and 
the  symptoms  abate  while  the  skin  reaction  shows 
marked  acidity,  it  is  an  indication  to  continue  pyretic 
treatment,  as  otherwise  we  shall  have  prolonged  con- 
valescence and  liability  to  relapse.  I  have  already 
called  attention  to  this  point,  but  it  is  so  important 
that  I  make  no  apology  for  repeating  it. 

I  have  previously  described  the  construction  of  the 
'  thermal  couch '  which  I  have  found  the  most  efficient 
means  of  giving  pyretic  treatment.  The  patient  is  in 
the  horizontal  position  and  surrounded  with  moist 
warm  air  (instead  of  vapour  or  steam),  and  the  tem- 
perature can  be  exactly  regulated  during  the  course  of 
the  bath,  which  is  an  important  factor.  This  is  done 


216     THE    NURSE'S    PART   IN    TREATMEXT 

not  only  by  altering  the  temperature  of  the  boiler, 
but  by  controlling  a  number  of  small  electric  lights 
placed  in  the  cover  of  the  couch. 

The  duration  of  the  treatment  is  determined  by  the 
moment  when  sweat  appears  upon  the  forehead  of  the 
patient.  If  this  should  occur  too  rapidly,  as  it  may 
do  in  patients  of  the  lactic-acid  diathesis  when  the 
skin  is  active,  it  is  an  indication  that  the  ordinary 
temperature  of  the  bath  (105°  F.)  is  too  high,  and  it  is 
reduced  at  the  next  bath.  If,  on  the  other  hand,  no 
sweat  appears  upon  the  forehead  in  twenty  to  twenty- 
five  minutes,  as  may  happen  during  the  first  days  of 
treatment  of  patients  with  suppression  of  the  cutaneous 
function,  the  bath  is  discontinued  and  repeated  the 
next  day  with  an  increased  amount  of  moisture  in  the 
air  of  the  bath.  It  is  very  seldom  that  cases  occur 
where  the  normal  functions  of  the  skin  are  not  restored 
within  three  days.  Twelve  days  is  the  longest  period 
I  have  known  before  the  skin  resumed  its  functions.* 

When  the  skin  acts  very  freely  it  is  often  a  good 
practice  to  turn  off  the  heat  ten  minutes  after  the 
patient  has  entered  the  bath.  Directly  indications  are 
given  that  the  skin  is  acting  freely,  the  temperature  of 
the  patient  is  taken.  While  this  is  being  done  the 
reactions  of  the  skin  are  tested.  As  a  routine  method 
that  of  the  forehead,  chest,  palms  of  the  hand,  and  soles 
of  the  feet  are  observed  and  recorded. 

The  temperature  before  and  after  the  treatment, 
together  with  the  four  skin  reactions,  being  recorded 


*  Nurses  should  be  specially  warned  against  attempts  to 
increase  the  efficiency  of  the  treatment  by  raising  the  tempera- 
ture of  the  bath.  Its  object  is  to  restore  and  stimulate  a  normal 
function,  not  to  obtain  sweating  by  exhausting  the  cutaneous 
nerves,  the  secondary  effect  of  which  is  to  diminish  their 
functional  activity. 


THE    NURSE'S    PART    IN    TREATMENT     217 

each  day,  make  a  chart  which  gives  exact  information 
concerning  the  patient's  progress.  Without  these 
observations  one  has  no  knowledge  of  the  actual  co 
ditions,  and  no  guide  to  the  number  of  treatments 
required.  It  is  as  a  result  of  the  information  thus 
obtained  that  one  realizes  the  large  number  of  baths 
which  are  necessary  to  free  the  tissues  from  the  excess 
of  lactic  acid  in  many  cases. 

At  intervals  during  the  treatment  specimens  of 
the  sweat  are  taken  for  microscopical  and  chemical 
examination.  I  find  the  most  convenient  method  is 
to  use  an  ordinary  teaspoon,  which  is  passed  over  the 
surface  of  the  skin,  and  the  contents  are  then  poured 
into  a  small  bottle,  labelled  with  the  name  of  the  patient. 
Some  distilled  water  from  the  vapour  of  the  bath  is 
mixed  with  the  sweat,  but  this  is  of  no  consequence. 
The  chemical  examination  is  of  importance,  especially 
in  cases  where  a  neutral  or  faintly  acid  reaction  persists. 
It  will  be  frequently  found  that  lactic  acid  exists  in 
large  quantities  but  is  neutralized  by  ammonia.  In 
a  large  number  of  acid  sweats,  ammonia  will  be  found. 

It  is  easier  to  train  nurses  to  give  baths  efficiently 
than  it  is  to  make  them  successful  manipulators  of 
crippled  joints.  It  does  not  follow  that  because  a 
nurse  has  had  a  course  of  training  as  a  masseuse  she 
will  secure  good  results  in  these  cases,  although  the 
manual  dexterity  she  may  have  gained  is  an  useful 
factor.  The  point  of  chief  importance  is  to  train 
nurses  to  recognize  the  degree  of  pressure  they  are 
using  when  they  handle  a  patient.  The  skin  pressed 
upon  the  subcutaneous  tissues  is  the  first  degree,  the 
skin  and  tissues  pressed  upon  the  muscles  is  the  second 
degree,  and  deep  pressure  of  all  the  tissues  on  the  bone 
is  the  third  degree. 


218     THE    NURSE'S    PART   IN    TREATMENT 

Having  secured  the  correct  pressure  in  any  particular 
condition,  they  must  be  taught  to  maintain  it  while 
moving  the  hand  either  laterally  or  in  a  circular  direc- 
tion, and,  while  the  movement  continues,  change  from 
one  degree  of  pressure  to  another.  They  will  thus 
obtain  the  muscular  sense  that  is  necessary  to  all 
manipulative  treatment.  The  second  most  important 
point  is  that  while  pressure  may  vary,  contact  must 
be  always  maintained. 

The  '  petrissage '  movement  so  much  favoured  by 
the  massage  school  is  very  objectionable  unless  it  is 
very  well  done.  The  staccato  pinching  of  the  muscles 
is  irritating  to  the  cutaneous  nerves.  Pressure  of  the 
third  degree  with  the  whole  hand  and  thumb,  alternating 
with  pressure  of  the  second  degree  and  passing  gradually 
into  one  another,  while  a  slight  rotatory  movement  of 
the  tissues  is  made  as  the  hand  glides  along  the  limb, 
is  more  efficient  and  is  soothing. 

But  in  the  class  of  cases  with  which  we  have  to  deal, 
resisted  movements  of  the  joints  are  much  more 
frequently  called  for  than  massage  manipulation. 
There  are  two  points  which  it  is  necessary  to  impress 
upon  nurses  in  giving  these  movements.  Each  move- 
ment must  be  complete,  the  flexion  must  be  carried 
as  far  as  is  possible  without  causing  unnecessary  pain, 
and  the  same  is  true  of  the  extension  movement.  When 
skill  is  obtained  in  the  treatment  of  contracted  joints, 
the  movement  commences  with  resistance  and  ends 
with  the  act  of  assistance,  the  greatest  care  being  taken 
not  to  carry  the  assisted  movement  too  far.  We  can 
only  obtain  the  help  of  the  patient,  which  is  the  most 
valuable  part  of  the  movement,  \\hile  he  has  the 
most  complete  confidence  in  the  manipulator. 

The  second  point  is  that  the  nurse  mu  t  be  instructed 


THE    NURSE'S    PART   IN    TREATMENT     219 

to  watch  the  patient  carefully  and  see  that  the  effort 
he  makes  is  only  the  result  of  the  contraction  of  the 
muscles  proper  to  the  movement.  I  have  seen  patients 
quite  exhausted  after  a  few  flexion  and  extension 
movements  of  the  limb,  because  at  each  effort  they 
have  contracted  a  large  number  of  muscles,  not  con- 
cerned in  the  movement. 

All  resisted  exercises  are  best  ordered  by  numbers, 
i.e.,  3,  6,  8,  or  10  to  each  joint.  In  no  case  should 
movements  be  continued  if  fatigue  is  produced.  Quite 
apart  from  contracted  joints,  many  rheumatic  patients 
have  defective  expansion  of  the  chest,  and  when  there 
is  free  movement  of  the  shoulder- joints,  chest-expansion 
exercises  are  of  great  benefit.  The  arms  of  the  patient 
are  raised  to  their  fullest  extent,  and  then  the  patient 
is  desired  to  draw  them  down  until  the  elbows  touch 
the  sides,  while  the  nurse  resists  the  movement. 

Personally,  I  order  the  patient  to  make  a  deep 
inspiration  as  the  arms  are  raised,  and  to  hold  the 
breath  during  the  resisted  movement. 

I  know  that  the  massage  school  is  opposed  to  the 
patient  holding  the  breath,  but  I  judge  by  the  results 
produced.  We  naturally  hold  the  breath  whilst  yawning, 
which  is  an  involuntary  effort  to  stimulate  the  heart. 
The  pulse  is  always  taken  before  such  movements,  and 
seldom  more  than  six  are  given,  when  the  pulse  is  again 
taken.  It  will  be  found  that  the  beat  has  increased  in 
volume,  and  become  slower,  as  a  result  of  the  treatment. 
If  it  should  become  quicker  it  shows  that  the  move- 
ment has  not  been  properly  given;  therefore  it  is 
necessary  to  have  the  pulse  taken  before  and  after  as 
a  routine  measure.  The  cause  of  failure  is  usually  that 
the  movements  have  been  performed  too  quickly — at 
least  four  normal  respirations  should  take  place  between 


220     THE    NURSE'S    PART   IN    TREATMENT 

each  movement.  A  single  inch  of  increase  in  the 
circumference  of  the  chest  represents  an  enormous 
addition  to  the  intake  of  oxygen  into  the  lungs  during 
the  twenty-four  hours,  so  the  importance  of  increasing 
the  chest  capacity  in  all  cases  where  there  is  defective 
oxidation,  cannot  be  overestimated.  Nurses  vary  very 
much  in  the  results  they  obtain  from  physical  treat- 
ment, and  as  a  rule  I  find  that  sympathy  is  a  more 
valuable  asset  to  such  nurses  than  strong  muscles. 

The  methods  I  have  described  have  been  the  means 
of  restoring  a  large  number  of  crippled  patients  to  a 
useful  life  ;  but  I  do  not  forget  that  these  results  are 
due  to  the  patient  labour  of  nurses  who,  in  doing  their 
work,  are  following  one  of  the  higher  and  most  useful 
branches  of  their  profession. 

One  good  reason  for  the  treatment  of  such  patients 
in  the  wards  of  general  hospitals  is  that  the  training 
which  renders  nurses  efficient  in  this  treatment  fits 
them  for  all  the  other  duties  of  nursing.  It  trains  their 
observation,  teaches  them  to  control  exactly  their 
muscular  activities,  and  gives  them  a  sense  of  responsi- 
bility and  a  pride  in  their  accomplishment  when  the 
task  is  completed. 


221 


INDEX. 


A  BDOMEN,  diagnostic  method 
£\     in  painful  affections  of   . .     208 
Acetylsalicylic   acid   in   sthenic 

cases  of  rheumatic  fever  116 
'  Acid  condition  of  the  blood  '  . .  32 
Acidity  of  excretions,  reason  for  70 

—  skin  in  rheumatism. .          . .       94 
Alcohol  and  arthritis  . .          . .     148 

—  in  gout  . .          . .          . .     146 

—  permanently     raising     body 

temperature        . .          . .     147 

—  and  uric  acid. .          . .          . .       72 

Ammonia,  great  amount  excreted 

by  skin,  and  lungs  81,  90 

—  increased     excretion     with 

active  exercise    . .          . .       28 

—  and   the    precipitation    of 

urates       . .          . .          . .       59 

—  in  sweat,  method  of  testing 

for 82 

of  patients  confined  to 

bed  82 

Ammonium  carbonate  as  the 

'  precursor  of  urea '       . .       21 

—  chloride  crystals  from  breath- 

ing on  'HC1         ..          ..       82 

and  the  precipitation  of 

urates   . .          . .          . .       68 

—  lactate,  alkaline  reaction  of        89 
excretion  a  cause  of  pre- 
mature grey  hair       . .     137 

how  formed        . .          .  .23,  27 

in  sweat  . .          . .          . .       89 

—  urate,  so  called         . .         . .       56 
Anaemia  and  haemoglobin  excess, 

diagnosis  between         . .     140 
Appendicitis,  dorsal  nerve  injuries 
causing  symptoms  simu- 
lating       . .          . .          . .     208 

—  gall-duct     pains     in     lithic 

patients  diagnosed  as  142,  208 
Arm,  neuritis  of,  due  to  lithate 

deposits  . .  . .  L  .  195 
'Arthritis  '  . .  . .  . .  150 

—  and  alcohol  . .          . .          . .     148 

—  deformans      . .          . .          . .     180 

nervous  shock   or  strain 

in  etiology       . .          . .     180 
treatment  182 


Arthritis  of  the  hip-joint         . .  185 

lumbar     plexus     injury 

causing  symptoms  of. .  204 

—  need  of  differentiating  cases  192 

prolonged  treatment      . .  131 

Asthenia  of  nerve-trunks         . .  197 
Asthenoxia — the  malaise  of  the 

lactic-acid  diathesis       99,  103 
Asthma,  connection  of  rheumatic 

gout  with          . .          . .  i77 

Atrophic  disease  of  hip- joint  . .  185 


BACTERIOLOGICAL  theory, 
harm  done  by,  in  chronic 
rheumatism     . .          . .     153 

of  joint  troubles. .          . .         2 

question  complicated  by     102 

of  rheumatism    . .          . .       99 

Bacteriology     and      rheumatic 

gout          175 

Baths,  non-use   of  by  our  an- 
cestors    . .          . .          . .     146 

—  steam  and  vapour  . .          . .     121 

—  Turkish  and  hot  air,   lactic 

acid  not  set  free  by  119,  121 
Bedclothes,  relation  to  gout  . .  139 
Bilious  attacks  in  lithic  patients  142 
Bird,  Golding,  on '  urate  of  soda '  48,  61 
Birds,  uric  acid  excretion  of  ..7i>  7- 
Blanket  pack,  hot  moist-method  126 
Blistering  in  chronic  synovitis  of 

knee-joint  . .  . .  188 

Blood,  '  acid  condition  of  . .  32 

—  proof  of  exciting  cause  of  gout 

not  in       . .          . .          . .     144 

—  relation     to     deposition     of 

lithates     . .         . .    _       13,  17 

—  sp.    gr.   of,    in   diagnosis   of 

lithic     and     lactic     acid 
diatheses  . .          . .         . .     140 

—  uric  acid  in  . .          . .          . .  56,  62 

(^  ALCULI  and  gravel  in  kidney    54 
V_y     —  uric    acid     and    phos- 
p  h  a  t  i  c,    vegetable 
dietary  and  . .       68 

Carbonate  of  ammonia  as  the 

'  precursor  of  urea  '      . .       21 


222 


INDEX 


Carbonic    acid    gas,    power    of 

breaking  up  urea  . .  83 
Cell,  cohesion  of  dead  and  living  21 

—  dead,  effect  of  lactic  acid  on       51 
origin  of  urea  in  the     . .        20 

—  —  study  of  the  physical  and 

chemical  conditions  of  22 
Cell-wall,  Kolliker  on  the  . .  43 

—  structure  of  . .          . .          . .       43 

Chemical  nature  of  the   urate, 

demonstration  of  . .       29 

—  and    physical   conditions    of 

the  dead  cell,  study  of  . .       22 

—  school,   conclusions  of,   and 

results      . .         . .         . .         2 

Chill  in  etiology  of  gonorrhoeal 

rheumatism         . .          . .     183 

—  physiological  effects  of       . .       96 

—  simple  method  to  overcome 

effects  of 129 

Chloride  of  ammonium,  combina- 

ation  with  lactic  acid  34,  88 
crystals  from  breathing 

on  HC1 82 

—  —  and  the  precipitation  of 

urates    . .          . .          . .       68 

—  sodium,  influence  of  urea  on      25 

in  sweat  . .          . .          . .       87 

Climate  in  etiology  of  rheumatism  100 
Clinical  facts       . .          . .          . .         9 

Clothing  in  relation  to  gout  and 

rheumatism  . .  . .  137 
Cold  as  factor  in  formation  of 

lithates  (see  also  Chill)  55,  137 
Cole,  S.  W.,  on  the  titration  test  56 
Colitis  due  to  nerve  injury  . .  209 
Complex  factors  in  joint  disease  190 
Crepitation  caused  by  presence 

of  lithates  . .          . .       16 

Croton     liniment     in     chronic 

synovitis          . .          . .     189 

rheumatic      gout      with 

asthma. .          . .          . .     177 

Crystals  of  ammonium  chloride 

from    breathing  on   HC1 

(Fig.  29)  . .         . .       82 

—  due   to   action   of  sulphuric 

acid    on    lactophosphate 

of  lime  (Figs.  18,  19)     . .       60 

—  —  '  urate  of  soda  '  (Golding 

Bird)  (Fig.  20)  ..       6r 

—  of  hydrate  of  lime  (Fi#.  13) . .       47 

—  lactic  acid  with  chloride  of 

sodium  (Fig.  7)  •  •          •  •       35 

—  lactophosphate  of  lime  (Figs. 

8-12)         46 

undergoing    modifica- 
tions (Figs.  21-27)         63 

—  'urate  of  soda'  (Figs.  14-17)       48 

—  urea  (Fig.  2) 23 


Crystals  urea  lactate  (Fig.  i) . .       23 

with  sodium  chloride  (Figs. 

3-6)       . .          . .  26,  29 

insoluble  in  strong  HC1 

(Fig.  28)     ..         . .       67 

DAGGER     crystals,    experi- 
ments with          . .          . .       25 
Diet    in    the   etiology    of   joint 

troubles    ....          . .         2 

—  gout    ..          ..  141,  146,  149 

—  rheumatic  fever       . .          . .     116 
Digestive  disturbances  in  gout. .      142 
Diphtheria  sometimes  diagnosed 

in  lactic-acid  diathesis  . .      101 
Drugs  as  physical  stimuli        . .       1 1 

ECZEMA,    due    to  excessive 
acid  excretion     . .  . .       94 

Electric  vibration  in  chronic  gout  171 
Electrical  diagnosis  in  lumbar- 
nerve  injuries     . .          . .     210 

—  treatment  in  lumbar  nerve 

injuries    ..          ..          ..  2ir 

Epidemics  of  rheumatic  fever  . .  99 

conditions    in    which 

they  could  occur  . .  103 
Eruptions,  artificial,  in  cure  of 

rheumatic-gout  headache  177 

Excretion . .         . .         . .          . .  79 

—  of  ammonia,  effect  of  exercise  81 
by  skin  and  lungs         . .  81 

—  importance  of  the  skin  in  . .  79 

—  of  products  of  tissue  meta- 

bolism, the  skin  the  great 
organ  of  . .          . .         . .         6 

Excretions,  reason  for  acidity  of      70 
Exercise,  active,  a  valuable  form 

of  pyretic  treatment     . .      129 

—  in  course  of  pyretic  treatment   125 

—  defective,    and   the  elimina- 

tion of  lithates  . .          . .       54 

—  effect  on  excretion  of  lithates      72 

—  increased   excretion   of   am- 

monia with         . .          . .       28 

—  lactic  acid  increased  by      . .       33 

—  and  proteid  metabolism     . .       80 

—  results  in  sedentary  men  71,  80, 134 

—  vigorous,  rise  of  temperature 

during,  role  of  skin  in    . .       85 
Exercises  in  chronic  rheumatism     158 

—  training  of  nurses  in. .          ..     218 

FATIGUE,    accumulation    of 
lactic  acid  in  muscle  in  . .       33 
Favre's  analysis  of  secretion  of 

skin          . .          •  •          •  •       87 
Fever,     continued,     importance 
of  observing  skin  reactions 
in  ..          ..         ..         ..215 


INDEX 


223 


Fever,  danger  of  suppressing  . . 

—  as    a    normal    physiological 

process 
—  therapeutic  agent     . . 

—  value  in  the  cure  of  rheuma- 

tism 
Fluid  intake  in  relation  to  gout 

140, 

Food,  excessive,  as  cause  of  gout 
Foods,  how  effecting  increase  of 

uric  acid 

Foot-bath  pack — method 
Forbes,   Murray,   on  lithic  acid 

in  the  blood 
Foster,  Sir  Michael,  on  lactic  acid 

protein  metabolism  . . 

— urea  in  urine 

Funke's  analysis  of  secretion  of 

skin 


PAGE 

117 


no 
no 


142 

I48 

72 
126 

56 
31 

4 
24 

87 


208 
62 
56 
42 
20 
56 

139 
136 


3 

183 
183 


/~*  ALL-DUCT,  pain  in,  in  lithic 
vJT     patients      .  .          .  .       142, 
Garrod  on  urate  of  soda  48 

—  uric  acid  in   the  blood     .  . 
Genesis  of  the  lithate  .  .          .  . 

—  urate  .  .          .  .         .  .          .  . 

—  uric  acid        .  .          .  .          .  . 

Germany,  reason  for  relatively 

little  gout  in       .  .          .  . 
Giddiness  a  symptom  of  gout    75, 
Gonococcus  and  arthritic,  sym- 

ptoms      .  .          .  .          .  . 

—  conditions  weakening  resist- 

ance to  attack  of          .  . 
Gonorrhoea!  rheumatism  .  . 

--  lactic-acid  diathesis  and 
--  modified  vaccine  method 

in          ......      184 

Gout,    action    of  lactic   acid   in 

causation.  .          .  .  142 

—  acute,  ancient  views  concern- 

ing origin  of    .  .          .  .        13 
--  Does  it  attack  a  healthy 

joint  ?    .  .  .  .  .  .        13 

—  Is  the  poison  conveyed  by 

the  blood  ?  13,  17 

—  the   two  clinical  concep- 

tions of..          ..          ..       13 

—  alcohol  in       .  .          .  .          .  .      146 

—  badly-warmed  houses  and  .  .      138 

—  bedclothes  in  relation  to   .  .      139 

—  chronic,  diagnosis     .  .          .  .      169 
--  need   of  prolonged  treat- 

ment     .  .          .  .          .  .      131 

--  pyretic  treatment  .  .      170 

—  common  in  women  .  .          .  .      137 

—  deficient  intake  of  fluids  in 

causation  .  .         .  .          .  .     140 

—  delusion  of  port-wine  drinking 

as  cause    .  .         .  .          .  .     146 


Goat  diet  in        . .  141,  146,  149 

—  digestion  in  . .          . .          . .     141 

—  evidence    of   local    cause    of 

chemical  action  . .          . .     144 

—  excessive  food  as  cause  of  . .      148 

—  headache,  bilious  attacks,  and 

gall-duct  pain  in  . .      142 

—  insufficient  clothing  causing       137 

—  kidney  impairment  and      . .      135 

—  lactophosphate  of  lime   and 

not  uric  acid  the  cause  of 
symptoms  . .          . .       75 

—  lithate  formation  not  neces- 

sarily followed  by         . .     133 

—  lithates  in  joints  of  persons 

with  no  symptoms  of    . .        14 

—  and  the  lithic  diathesis      . .      132 

—  physiological  conditions  caus- 

ing chemical  changes  in 
lithates     . .          . .          . .     142 

—  reasons    for    prevalence    in 

Great  Britain      . .          . .     137 

—  relation  to  kidney  impairment     54 

—  rheumatic     (see     Rheumatic 

Gout)        . .          . .          . .     172 

—  sedentary  life  and  exercise  in     135 

—  tobacco  smoking  and         . .     148 

—  want  of  cleanliness  and  exer- 

cise as  cause       . .          . .     146 
Gouty  patients,  the  typical  hand- 
shake of  . .          . .          . .     132 

—  and     rheumatic     patients, 

difference  in  skin  reactions  of  91 
Gravel  and  stone  in  kidney  . .  54 

HEMOGLOBIN  deficiency 
sometimes  a  factor  in 
etiology  of  rheumatism . .  107 

—  e>:cess  and  ana?mia,  diagnosis 

between    . .         . .         . .  140 

Haig,  method  of  experiments  of  77 

—  on  uric  acid   . .          . .          . .  76 

Hair,  tendency  to  turn  grey  or 

white  in  lithic  diathesis. .  136 
Handshake,  typical,  of  lithic  and 

rheumatic  patients  . .  132 

Headache  in  lithic  patients  . .  142 

—  rheumatic  gout        . .          . .  176 
Heart  disease,  effect  of  pyretic 

treatment  ..          ..     122 

and  rheumatic  fever 

106,  in,  117 

—  pain    in   region    of,    due    to 

dorsal  nerve  injury       . .     207 
Heat,  evolution  of,  in  combina- 
tion of  lactic  acid  with 
ammonia  . .         . .          . .     108 

Heating,  domestic,  in  preven- 
tion of  gout  and  rheuma- 
tism . .  . .  . .  138 


224 


INDEX 


PAGE 

Heating,  domestic,  waste  and 
inefficiency  of  present 
systems  . .  138 

Hip- joint,  arthritis  of  . .          . .      185 

—  atrophic  disease  of  . .          . .     185 

—  disease,  pain  in  knee  a  reflex 

sympton  of        ..          ..     190 

—  hypertrophic  disease  of      . .     187 

—  spasm  of  muscles  of,  through 

lumbar-plexus    injuries. .     204 
Hot  moist  blanket  pack — method  126 
Houses,    insufficiently   warmed, 
a    cause    of     gout    and 
rheumatism         . .         . .     138 

Human  body  as  a  heat -producing 

machine    . .          . .          . .     118 

Hydrate  of  lime,  crystals  of    . .       47 
Hypertropbic    disease    of    hip- 
joint         187 

TNFECTIOUS    disease,    rheu- 
A         matism  as  an       . .         99,  102 
Influenza  bacillus  and  rheuma- 
tism         . .         •  •          • •     100 

—  sometimes  diagnosed  in  lactic- 

acid  excess         . .         . .       98 

JOINT  changes,  difference    in 
J      chronic     rheumatism    and 

rheumatoid  arthritis      . .     152 

—  disease,  complex  factors  in. .     190 
conclusions  of  the  chemical 

school  on         . .         . .         2 

difference  between  sym- 
ptoms and  disease  . .  9 

due  to  lesions  of  central 

nervous  system  . .  191 

each  case  a  physiological 

problem  . .  . .  8 

lithates  in  persons  with 

no  symptoms  of  . .  14 

—  manipulation,     training     of 

nurses  in  . .         . .         : .     217 

—  symptoms  not  invariable  in 

rheumatic  gout  . .          . .     176 
Joints,    breaking    down    under 

anaesthetic          . .         . .     160 

—  method    of    examining    for 

presence  of  lithates      . .       16 

TT'IDNEY   calculus,  diagnosis 
J\.     from  lumbar  neuralgia  . .     201 

—  impairment,  relation  to  gout 

54,  135 

Kidneys,  functions  of  skin  per- 
formed by  . .          . .     136 
Knee,  chronic  synovitis  of      . .     188 

—  giving    way    of,    through 

lumbar-plexus  injuries  . .     203 


Knee,  pain  in,  reflex  symptom 

of  hip  disease    . .          . .     190 
Kolliker  on  the  cell-wall         . .       .13 

T    ACTATE     of    ammonium, 

J__/     alkaline  reaction    of       . .       89 

excretion     a     cause     of 

premature  grey  hair  . .     137 

—  " —  how  formed         . .  23,  27 
in  sweat  . .         . .         . .       89 

—  urea  crystals  . .         . .         . .       23 

Lactates,    large    proportion    in 

excretions  . .          . .       34 

Lactic  acid          . .          . .         . .       31 

action  in  causation  of  gout    142 

dislodgement  of  dead 

cells  . .          . .       45 

affinity  for  lime  . .          . .       44 

the  author's  test  for      . .       38 

in  causation  of  stiffness 

and  rigor  mortis        . .       37 

combination  with  sodium 

chloride  . .  35,  88 

deficient  elimination  of..       53 

diathesis  . .         . .          . .       94 

diphtheria   sometimes 

diagnosed  in         . .     101 

— in  etiology  of,  gonor- 

rhoeal  rheumatism       183 
pharyngitis  and  tonsil- 
litis in        . .          . .     loi 

effect  on  the  dead  cell  . .       51 

temperature,  of  liberat- 
ing . .         . .         . .     108 

excess    causing    rise    of 

temperature        during 
exercise  . .          . .     109 

in  sweat  in  apparent 

health        . .         . .       94 

excretion,  effect  of  '  chill ' 

on         . .         . .         . .       96 

excessive,  a  cause  of 

eczema       . .          . .       94 

' influenza '      and 

'typhoid'  some- 
times diagnosed 
in  . .  . .  98 

factors       concerned       in 

checking  elimination..     107 
free,  pulse  and  tempera- 
ture     in      diagnosing 
presence  of     . .         . .     215 

great  affinity  for  animal 

tissues  . .          . .  34,  38 

and  lithic  diatheses,   sp. 

gr.  of  blood  in  diagnosis     140 

a  normal  constituent  of 

urine 37 

peculiarities  of  combina- 
tions of  . .  35 


INDEX 


225 


Lactic  acid,   a  product  of  mus- 
cular metabolism  . .       33 
secretion  following  nerve- 
trunk  lesions  . .          . .      198 

Sir  M.  Foster  on. .          . .       31 

Uffelmann's  test  for      . .       38 

Lactochloride  of  ammonium    . .       35 
Lactophosphate  of  lime,  action 

of  sulphuric  acid  on  60 

the   cause   of   symptoms 

of  gout . .          . .          . .       75 

crystals  undergoing  modi- 
fication . .         . .          . .       63 

described  as  urate  of  soda      48 

—  effect  of  defective  excretion  54 

—  illustration  of  crystals     46,  47 
omnipresence  in  body  . .       75 

—  structure  of        . .          . .       45 

—  in    sweat    of    rheumatic 

patients  . .  . .  89 

when  soluble  or  insoluble  53 

Leg,  apparent  shortening  of, 

from  lumbar-plexus  injury  204 
Lime,  its  binding  action  in  the 

cell-wail    . .          . .          . .       44 

—  as  a  food  in  agriculture  and 

medicine  . .          . .          . .     165 

—  hydrate  of,  illustration  of  . .       47 

—  lactophosphate  of  (sec  Lacto- 

phosphate) 

—  salts    and    urates,     striking 

difference  between        . .       46 

—  in  water,  effect  in  gout  and 

rheumatoid  arthritis    141,  164 
Lithate  formation  due  to  absence 
of    free    lactic    acid    in 
lymph  space      . .          . .     132 

following    nerve-t  r  u  n  k 

lesions  . .          . .     198 

—  genesis  of  the  . .          . .       42 

—  physical  causes  of  formation 

of  deposits          . .          . .       49 

—  role  of  the  great  lymph  space 

in  its  formation  . .          . .       50 

—  term  preferable  to   '  urate  '       42 
Lithates,    cold    and  subnormal 

temperature  as  agents  . .       55 

—  deficient  fluid  intake  causing 

formation  of       . .          . .     140 

—  in  joints  of  persons  without 

symptoms  . .  14,  52 

—  method   of  examining  joint 

for  presence  of  . .          . .       16 

—  neuritis  of  arm  due  to       . .     195 

—  physiological     conditions 

causing  chemical  changes     142 

—  reduced  in  size  in  an  attack      16 

—  in    tissues    not     necessarily 

followed  by  gout  . .     133 

—  usually  in  the  less  active  joints     54 


Lithic  diathesis,  the      . .          . .  132 

gall-duct  pains  in          . .  208. 

and  lithitis,  definition  of  15 

—  . —  skin  reaction  in. ,          . .  91 
tendency  for  hair  to  turn 

grey  in. .          . .          . .  136 

the  typical  handshake  of  132 

—  and  lactic  acid  diathesis,  sp. 

gr.  of  blood  in  diagnosis  140 

—  patients,     alcohol    and    the 

incidence  of        . .          . .  148 

two  classes  of     . .          . .  134 

Lithitis,  chronic  (see  also  Gout)  169 
Liver  and  the  formation  of  uric  acid  57 

—  obscure  pains  over,   due  to 

dorsal-nerve  injury        . .  207 

—  urea  not  specially  manufac- 

tured by  . .          . .          . .  23 

Lumbar   neuralgia,    traumatism 

in  etiology           . .          . .  200 

—  plexus,  examination  of       . .  200 
injuries,  electrical  diagno- 
sis and  treatment      . .  211 

— knee  giving  way  in  . .  203 

spasm  of  hip  muscles  from  204 

Lymph,     Garrod's     experiment 

with  acetic  acid  . .          . .  56 

—  proof  of  exciting  cause  of  gout 

not  in       . .          . .          . .  144 

—  space,     chemical     changes 

occurring  in        . .          . .  50 

role  in  formation  of  lithate  50 

subcutaneous,  importance 

in  excretion     . .          . .  5 

MASSAGE,  special,  training  of 
nurses  in  . .          . .     217 

Meat,  red,  and  uric  acid         . .       72 
Mental  depression  due  to  check 

to  lactic  acid  excretion  . .       97 
Metabolism,  importance  of  subcu- 
taneous lymph  space  in. .         5 

—  little    influence    of    food    or 

drugs  on  . .          . .          . .  5 

—  protein,  Sir  Michael  Foster  on  4 
Milk  diet  in  rheumatic  fever    ..  116 
Mineral  baths     . .          . .          . .  130 

Mountain  climbing,  physiological 

effects  of  . .          . .          . .       80 

Movements,  passive  and  active, 

in  chronic  rheumatism  . .      158 

—  resisted,  training  of  nurses  in     218 
Muscular    action,    increased,    in 

etiology  of  rheumatic  fever  107 

—  metabolism,  lactic  acid  a  pro- 

duct of     . .          . .          . .  33 

—  rheumatism   . .          . .          . .  193 

—  —  diagnosed  as  neuritis     . .  194 

—  stiffness,  lactic  acid  in  causa- 

tion of  . .          . .       37 

15 


226 


INDEX 


NERVE-SUPPLY  exhaustion 
in  etiology  of  rheumatic 
fever         . .         . .         . .     107 

Nerve-trunks,  asthenia  of       . .     197 
symptoms  . .          . .     199 

—  rheumatism  in  sheath  of 

193,  195,  197,  199 
Nervous  shock  or  strain  in 

etiology  of  arthritis  defor- 

mans        . .          . .          . .     1 80 

Neuralgia,  lumbar,  diagnosis 

from  renal  calculus  . .  201 

traumatism  in  etiology. .  200 

Neurasthenia  due  to  check  to 

lactic-acid  excretion  . .  97 
'  Neuritis  '  . .  . .  . .  193 

—  of   arm   due    to   diminished 

blood-supply  . .  . .  197 
lithic  deposits  . .  195 

—  improper  application  of  teim     212 

—  muscular    rheumatism    dia- 

gnosed as . .          . .          . .     194 

—  rarity  of  inflammation  of  nerve  193 

—  traumalgia     and     traumas- 

thenia       ..         ..         ..     212 

—  use  of  term  contra-indicating 

necessary  treatment  . .  198 
Nitrogen,  effect  of  in  dietary  of 

soldiers     . .          . .          . .         2 

—  excess  as  cause  of  joint  trouble       2 

—  great    amount    excreted    by 

skin  and  lungs  . .  . .  81 
Nurse's  pait  in  treatment  ..  213 
Nurses,  special  training  necessary 

213-218 


OVARY,     removal     of,      in 
asthenia  of   nerve-trunks 
Oxidation,  imperfect,  in  etiology 

of  rheumatic  fever       .'.     107 


209 


PACK,  foot-bath — method  . .     126 
—  hot    moist    blanket  — 

method      . .         . .     126 

Pharyngitis      with      lactic-acid 

diathesis  . .          . .          . .      101 

Phosphate  of  lime  calculi,  vege- 
table dietaiy  and          . .       68 

its  purpose  in  the  cell-wall      44 

Physical  and  chemical  conditions 

of  the  dead  cell,  study  of      22 
Port  wine  and  gout      . .          . .     146 

Prognosis,    skin   reaction   infal- 
lible in  rheumatism 

104,  113,  128 
Protein  metabolism,  Sir  Michael 

Foster  on  . .        . .          . .         4 

Pulse,     rapid,     with    moderate 

temperature        . .          . .     215 


PAGE 

Pulse,  relatively  slow  in  iheuma- 

tism           . .          . .         98,  109 
Putrefaction,    lactic   acid   as   a 

preventive           . .          . .  34 

Pyretic  treatment          ..          ..  117 

active  exercise  a  valuable 

form  of             . .          . .  129 

•  administration  of  vaccines 

a  form  of        . .          . .  130 

appliance     for     treating 

patients  in  bed          . .  121 

author's     appliance     for 

and  its  '  improvements  '  n& 

in  chronic  gout  . .          . .  170 

rheumatism   . .        151,  157 

effect  on  chronic  V.D.H.  122 

•  exercise  in  course  of     . .  125 

foot-balh  pack   ..          ..  126 

in   gonorrhoeal   iheumat- 

ism       . .          . .         . .  184 

hot  moist  blanket  pack. .  126 

length  of  course. .          . .  125 

method    of    using    moist 

warm  air         . .          . .  120 

mineral  baths     . .          . .  130- 

in  muscular  rheumatism  194 

need  of  employment  by 

practitioner     . .          . .  125 

-  —  nurse's  pait  in    . .          . .  213 

in  rheumatoid  arthritis. .  166 

skin  reaction  the  indica- 
tion of  cure     . .          . .  12} 

spinal    irritation    from — 

prevention       . .          . .  124 

thermal  couch  described  121 

Turkish  and  hot  immer- 
sion baths  useless     119,  121 
value,  and  conditions  indi- 
cating it          . .          . .  117 
vapour  baths      . .          . .  127 

RENAL     calculus     diagnosis 

from  Jumbar  neuralgia    . .  201 

Rheumatic  fever           . .          . .  106- 

the  fever  a  physiological 

process             ..         ..  u<> 

heart  disease  and  106,  in,  117 

milk  diet  in        ..          ..  116 

—  —  misleading  symptoms  of 

cure      ..          ..          ..  113 

—  —  recovery    occasionally 

without  treatment     ..  112 

—  —  relapse  not  occurring  after 

complete  treatment  . .  113 

sthenic  and  asthenic  cases  n& 

symptoms  . .  . .  106 

three  factors  concerned 

in   production..          ..  107 

—  gout    . .          . .          . .         . .  172 

connection   with    asthma  177 


INDEX 


227 


Rheumatic  gout,  joint  symptoms 

not  invariable  in          .. 

—  micro-organisms    compli- 

cating  .  .          .  .          .  . 

—  recurring   and   persistent' 

headache  in     .  .          .  . 

-  —  symptoms  ..          .. 

--  treatment  .  .          .  . 

—  and   gouty   patients,    differ- 

ence in  skin  reactions  of 

91, 

—  patients,  reason  for  treating 

in  general  hospitals       .  . 
Rheumatism,  acidity  of  skin  in 

—  badly-warmed  houses  and  .  . 

—  chronic  .  .          .  .          .  . 

—  breaking  down  joints  in 
--  cause  of  muscle  wasting 

—  a  curable  disease          .  . 
--  diagnosis      from      other 

chronic  joint  diseases.  . 

—  diagnosis   of   rheumatoid 

arthritis  from.  .          .  . 
--  etiology    .  .          .  .          .  . 

—  exercises  for        .  .          .  . 

—  exposure     to    cold  in 

.    etiology  .  .          .  . 

—  ill  effect  of  vaccines    153, 
--  passive  and  active  move- 

ments in          .  .          .  . 

—  pyretic  tieatment         151, 
--  secondary    to    iheumatic 

fever     .  .          .  .          .  . 

—  definition  and  etiology       .  . 

—  epidemics   of,    conditions  in 

which  they  could  occur.  . 

—  gonorrhceal    .  .          .  .          .  . 

—  —  lactic  acid  diathesis  and 
--  modified  vaccine  method 

in          .  .          .  .          .  . 

—  as  an  infectious  disease      99, 

—  improvement  in  joint  sym- 

ptoms not  sign  of  cure 

104,  113, 

—  and  the  lactic-acid  diathesis 

—  liability  to  follow  a  sprain.  . 

—  muscular        .  .          .  .          .  . 

--  diagnosed  as  neui  itis     .  . 

—  natural  tendency  to  recovery 

—  need  of  prolonged  treatment 

—  pyretic  treatment     ..          .. 

—  reasons    for     prevalence    in 

Gieat  Britain      .  .          .  . 

—  relatively  slow  pulse  in        98, 

—  seasonal   incidence   of  .  . 

—  in  sheath  of  nerve-trunks  193, 
---  sciatica  due  to  .  . 

—  skin    reaction    infallible  in 

prognosis..  104,  113, 

—  subacute  articular    .  .          .  . 


PAGE 

176 
i75 

176 
172 
175 

125 

220 
94 
138 
150 
160 
152 
153 

151 

162 
151 
158 

3 
156 

157 
157 

163 
94 

103 
183 
183 

184 
102 


128 

94 

33 

193 

194 

117 

131 

117 

137 
109 
100 
195 
195 

128 
163 


Rheumatism,  subacute,  vaccines 

in              . .          . .          . .  169 

—  of  tendons     . .            193,  195,  199 
Rheumatoid   arthritis    . .          . .  162 

—  chronic  rheumatism  dia- 
gnosed as        . .          . .  152 
diagnosis  . .         . .          . .  162 

—  — -  —  of  chronic  gout  from . .  169 

—  —  fluid  in  joints  in. .          . .  167 

—  —  lime  deficiency  in          . .  164 

—  pyretic  treatment          . .  166 
rest  and  movements  in. .  166 

—  the  typical  handshake  of  132 

vaccines  in          . .  168 

Rigor    mortis,     lactic     acid    in 

causation  of       . .          . .  37 
Rupia     following     vaccine      in 

gonorrhceal  rheumatism  185 

SACRAL     plexus     injuries, 
symptoms  . .          . .     206 

Salicylates,  serious  results  from       in 

—  when  not   dangerous          . .     1 1 6 
Schafer  on.  exeicise  and  proteid 

metabolism          . .          . .       80 

—  uric  acid        . .          . .          . .       69 

Schottin's  analysis  of  secretion 

of  skin 87 

Sciatica  due  to  rheumatism  in 

sheath  of  nerve  . .  . .  195 

Scoliosis  simulated  by  lumbar- 
plexus  injuries  . .  . .  204 

Sedentary  habits  and  exercise, 

results  of..  ..  71,  80,  134 

Sex  incidence  of  gout    . .          . .      137 

Shoulder,  neuritis  due  to  lithic 

deposits  in  . .  . .  195 

Skin,  acid  reaction  in  apparent 
health 

— rheumatism    . . 

—  adhesion  of  dead  cells  to    . . 

—  alkaline  and  acid  reactions  of 

—  dry,  with  persistent  subnormal 

temperature         . .          . .       52 

—  and  the  elimination  of  waste 

products  . .          . .          . .       79 

—  excretion,  effects  of  '  chill '  on      96 

—  functional  inactivity  as  cause 

of  disease  . .          . .       85 

—  functions       performed      by 

kidneys     . .          . .          . .     136 

—  the  great,  excretory  organ  of 

products  of  tissue  meta- 
bolism     . .          . .          . .         6 

—  inactive,  effect  on  kidneys..       54 

—  insufficiently    recognized    as 

organ  of  secretion         . .       84 
— -     reaction,  difference  in  rheu- 
matic and  gouty  patients 

9i,  125 


228 


INDEX 


Skin    reaction,    importance    in 

diagnosis               . .          . .  98 

infallible  in  prognosis  of 

rheumatism    102,    113,  128 

—  as  a  source  of  heat  . .          . .   6,  86 
Sodium  chloride,  influence  of  urea 

on         . .          . .          . .  25 

in  sweat  . .          . .          . .  87 

—  urate,    absence  in  body    . .  28 

Ganpd  on  . .          .  .48,  62 

Golding  Bird  on . .          . .  48 

non-existence  in  the  body  48 

Sore     throat     with     lactic-acid 

diathesis  . .         . .         . .  101 

Spa  treatment    . .          . .          . .  130 

Spinal  irritation  after  pyretic 

treatment — prevention  . .  124 

Steam  and  vapour  baths  . .  121 
Stiffness,  lactic  acid  in  causation 

of 37 

Stimuli,  physical,  drugs  as  . .  n 
Stomach,  obscure  pains  over, 

due  1o  dorsal -nerve  injury  207 

Sugar  and  uric  acid  . .  . .  72 

Sulphur  vapour  baths  . .  . .  128 
Sweat,  acidlactate  of  ammonium 

in  . .          . .          . .          . .  89 

—  alkaline  and  acid  reactions  of  90 

—  ammonia  in,  after  exercise. .  81 
in  patients  confined  to  bed  82 

—  chemical  analyses  of  87 

—  chemical   composition   influ- 

enced   by    processes    in 

tissues  immediately  below  92 

—  difference  of  reaction  in  rheu- 

matic and  gouty  patients  91 

—  method     of     collecting     for 

examination        . .          . .  217 
testing  for  ammonia     . .  82 

—  of  rheumatic  patient  {Fig.  31)  89 

—  showing  combination  of  urea 

with  NaCl  (Fig.  30)      ..  88 
Sweating,     two    physiologically 

distinct  forms  of  86 
Symptoms  and  disease,  import- 
ance of  differentiating  . .  9 

—  the  reaction  of  the  organism 

against  disease   . .          . .  10 

Synovitis,  chronic,  of  knee-joint  188 

^TEMPERATURE,  alcohol  as 
J.        agent    in    permanently 

raising      . .          . .          . .     147 

—  bodily,  physiology  of         ..     118 

—  in  chronic  rheumatism       . .     151 

—  diminished    by    increasing 

external  heat      . .          . .     120 

—  effect  of  liberation  of  lactic 

acid  on     . .         . .          . .     108 


Temperature,     as    a    guide    in 

pyretic  treatment  . .      123 

—  rise  after  exercise     . .          . .       81 
not     necessarily     patho- 
logical  . .          . .          . .      109 

—  subnormal,  as  agent  in  pro- 

duction of  lithates     . .       55 

association  with  inactivity 

of  skin  . .          . .         . .       85 

enormous  impoitance  not 

recognized       . .          . .     109 

in  healthy  men  . .          . .  7,  50 

instruction  of  nurses  re- 
garding..        ..          ..     2r3 

rise   to    normal,    a    true 

fever     . .          . .          . .     124 

—  variations  in,  nurse's  part  in 

observing. .          . .          . .     214 

—  various  ways  of  raising      . .     r  r  8 
Tendons,    overstrain    of,    sym- 
ptoms of  . .          . .          . .     199 

—  rheumatism  of    193,  rgs,  rg7,  199 
Test  for  lactic  acid       . .          . .       38 
Thermal  couch,  description  of . .      121 

nurse's  part  in  use  of    . .     215 

Tissue   metabolism,    importance 

of    subcutaneous    lymph 
space  in    . .         . .          . .         5 

Titration  method  of  testing  uric- 
acid  excretion     . .          . .       58 

Tobacco  smoking  and  gout      . .     148 
Tonsillitis,  follicular,  with  lactic- 
acid  diathesis      . .          . .      101 

Trauma  in  etiology  of  '  neuritis  '  198 
Traumalgia  and  traumasthenia  212 
Treatment,  nurse's  part  in  . .  2r3 
Turkish  baths,  lactic  acid  not 

set  free  by          . .  rrg 

'  Typhoid '  sometimes  diagnosed 

in  lactic-acid  excess      . .       98 

UFFELMANN'S  test  for  lactic 
acid          37 

Urate  of  ammonium :    does  it 

exist  ? 56 

—  soda,  absence  of  evidence  of 

existence  in  body     . .       28 

—  —  Garrod  on  . .  48,  62 
Golding  Bird  on  . .          . .       48 

lactophosphate     of     lime 

described  as    . .          . .       48 
non-existence  in  the  body      48 

—  demonstration    of    chemical 

nature  of  . .         . .          . .  29 

—  genesis  of                  . .          . .  20 
Urates  (see  also  Lithates)         . .  r4 

—  ammonia  and  the  precipita- 

tion of  . .          . .       59 

—  biurate  and  quadriurate     . .       42 


INDEX 


229 


Unites  and  lime  salts,  striking 

difference  between        . .        46 

—  of    silver    and    ammonium, 

chemical  mistakes         . .        77 
Urea  broken  up  into  elements 

by  COz 83 

—  carbonate   of   ammonia   the 

'  precursor  '  of   .  .          . .        21 

—  excretion  through  the  skin         79 

—  formed  in  large  quantities  in 

muscles  . .          . .        82 

—  tissues  as  normal  product 

•  if   metabolism  .  .        23 

—  great  affinity  for  acids       . .        23 

—  influence    on    formation    of 

chloride  of  sodium  crystals    25 

—  lactate  crystals        .  .  .  .        23 
-  method  of  preserving  alka- 
linity of  blood   .  .  .  .        28 

—  not  contained  in  uric  acid. .        69 

—  as    a    necessary    and    safe- 

guarding  agent. .  . .        30 

—  its  origin  in  the  dead  cell  .  .        20 

—  quantity  passed  in  urine    . . 

—  Why  is  it  not  found  in  the 

muscles  i 

Uric  acid  in  the  blood. .          •  .56,  62 
—  difficulties  created  by 

false  conception  .  .        74 

—  (iarrod  on     . .          . .        56 

—  conclusion  that  it  contains 

no  urea  .  .  . .        69 

—  conditions  governing  for- 

mation  as  product  of 
human    body. .          . .        69 

—  excretion  of  birds  71,   72 

—  remarkable     mistake 

concerning  . .        24 

—  acid,  genesis  of       . .          . .        56 

—  —  Haig  on  . .          76 

-  liver  and  the  formation  of     57 

—  -  Schiifer  on          . .          - .        69 


Uric  acid,  synthetic  experiments 

62,  64 

theory,  the  fundamental 

error  of          . .          . .       71 
-     in    urine,    method    of 
demonstrating  presence 

of         57 

What  purpose  serving  in 

economy  of  nature  ?  . .        73 
Urine,    absence    of   crystals    of 

urea  in     . .          . .          . .        24 

—  the  author's  test   for  lactic 

acid  in     . .          . .          . .        38 

—  lactic  acid  a  normal  constitu- 

ent of  .'.          . .        37 

—  test  for  uric  acid  in .  .          . .        57 

VACCINE  method,  modified, 
in  gonorrhoeal  rheumatism  184 

—  therapy   a    form   of   pyretic 

treatment  . .          . .      130 

Vaccines,  in  rheumatoid  arthritis  168 

—  useless  and  harmful  in  chronic 

rheumatism  . .  153,  156 
Valvular  disease  of  heart,  effect 

of  pyretic  treatment  on  122 

Vapour  baths — method  . .  127 

—  and  steam  baths     ..          ..  121 
Vegetable  diet  in  gout. .          . .  141 
in     tendency     to     form 

calculi .  .  .  .          .  .        68 

WASTE  products,  non-exist- 
ence of  . .          . .          . .          5 

Water,  hard,  and  gout  . .      141 

—  soft,  and  rheumatoid  arthritis    164 
Women,    insufficient-  clothes   a 

cause  of  gout  in . .          . .      137 


JOHN    UK1GHT    AND    SONS    LID.,    PK1NTEKS     \ND    HUliMSHliRS, 


University  of  California 

SOUTHERN  REGIONAL  LIBRARY  FACILITY 

405  Hilgard  Avenue,  Los  Angeles,  CA  90024-1388 

Return  this  material  to  the  library 

from  which  it  was  borrowed. 


OlOCTiG  1995 
MAY  05tt» 


MAY  1 1 198b 
DEC  1  9 1995 


I 


PRINTED  IN   U.S. 


CAT.      NO       24      161 


°f  gout, 
arthritis 


W6?2p 
1922 

Wilde,  Percy. 

Physiology  of  gout,  rheumatism,  and 
arth\ritis 


MEDICAL  SCIENCES  LIBRARY 

UNIVERSITY  OF  CALIFORNIA,  IRVINE 

IRVINE,  CALIFORNIA  92664 


3  1970  01643  5882 


